@article{RN1609,

title = {Supramolecular Polymerization of Triarylamine-Based Macrocycles into Electroactive Nanotubes},

author = {F. Picini and S. Schneider and O. Gavat and A. Vargas Jentzsch and J. Tan and M. Maaloum and J. M. Strub and S. Tokunaga and J. M. Lehn and E. Moulin and N. Giuseppone},

url = {https://www.ncbi.nlm.nih.gov/pubmed/33834779},

doi = {10.1021/jacs.1c00623},

issn = {1520-5126 (Electronic) 

0002-7863 (Linking)},

year  = {2021},

date = {2021-01-01},

journal = {J Am Chem Soc},

volume = {143},

number = {17},

pages = {6498-6504},

abstract = {A S6-symmetric triarylamine-based macrocycle (i.e., hexaaza[16]paracyclophane), decorated with six lateral amide functions, is synthesized by a convergent and modular strategy. This macrocycle is shown to undergo supramolecular polymerization in o-dichlorobenzene, and its nanotubular structure is elucidated by a combination of spectroscopy and microscopy techniques, together with X-ray scattering and molecular modeling. Upon sequential oxidation, a spectroelectrochemical analysis of the supramolecular polymer suggests an extended electronic delocalization of charge carriers both within the macrocycles (through bond) and between the macrocycles along the stacking direction (through space).},

note = {2021-02 (service chimie)},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN1616,

title = {A proteomic-informed view of the changes induced by loss of cellular adherence: The example of mouse macrophages},

author = {S. Ramirez Rios and A. Torres and H. Diemer and V. Collin-Faure and S. Cianferani and L. Lafanechere and T. Rabilloud},

url = {https://www.ncbi.nlm.nih.gov/pubmed/34048472},

doi = {10.1371/journal.pone.0252450},

issn = {1932-6203 (Electronic) 

1932-6203 (Linking)},

year  = {2021},

date = {2021-01-01},

journal = {PLoS One},

volume = {16},

number = {5},

pages = {e0252450},

abstract = {Except cells circulating in the bloodstream, most cells in vertebrates are adherent. Studying the repercussions of adherence per se in cell physiology is thus very difficult to carry out, although it plays an important role in cancer biology, e.g. in the metastasis process. In order to study how adherence impacts major cell functions, we used a murine macrophage cell line. Opposite to the monocyte/macrophage system, where adherence is associated with the acquisition of differentiated functions, these cells can be grown in both adherent or suspension conditions without altering their differentiated functions (phagocytosis and inflammation signaling). We used a proteomic approach to cover a large panel of proteins potentially modified by the adherence status. Targeted experiments were carried out to validate the proteomic results, e.g. on metabolic enzymes, mitochondrial and cytoskeletal proteins. The mitochondrial activity was increased in non-adherent cells compared with adherent cells, without differences in glucose consumption. Concerning the cytoskeleton, a rearrangement of the actin organization (filopodia vs sub-cortical network) and of the microtubule network were observed between adherent and non-adherent cells. Taken together, these data show the mechanisms at play for the modification of the cytoskeleton and also modifications of the metabolic activity between adherent and non-adherent cells.},

note = {2009/55},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN1612,

title = {Catestatin in innate immunity and Cateslytin-derived peptides against superbugs},

author = {F. Scavello and A. Mutschler and S. Helle and F. Schneider and S. Chasserot-Golaz and J. M. Strub and S. Cianferani and Y. Haikel and M. H. Metz-Boutigue},

url = {https://www.ncbi.nlm.nih.gov/pubmed/34341386},

doi = {10.1038/s41598-021-94749-6},

issn = {2045-2322 (Electronic) 

2045-2322 (Linking)},

year  = {2021},

date = {2021-01-01},

journal = {Sci Rep},

volume = {11},

number = {1},

pages = {15615},

abstract = {Chromogranin A (CgA) is the precursor of several antimicrobial peptides, such as Catestatin (Cts, bovine CgA344-364), initially described as a potent inhibitor of catecholamines. This peptide displays direct antimicrobial activities and contributes to immune system regulation. The aim of the present study is to investigate a designed peptide based on Cts to fight infections against superbugs and more particularly Staphylococcus aureus. In addition to Cateslytin (Ctl, bovine CgA344-358), the active domain of Catestatin, several peptides including dimers, D-isomer and the new designed peptide DOPA-K-DOPA-K-DOPA-TLRGGE-RSMRLSFRARGYGFR (Dopa5T-Ctl) were prepared and tested. Cateslytin is resistant to bacterial degradation and does not induce bacterial resistance. The interaction of Catestatin with immune dermal cells (dendritic cells DC1a, dermal macrophages CD14 and macrophages) was analyzed by using confocal microscopy and cytokine release assay. The dimers and D-isomer of Ctl were tested against a large variety of bacteria showing the potent antibacterial activity of the D-isomer. The peptide Dopa5T-Ctl is able to induce the self-killing of S. aureus after release of Ctl by the endoprotease Glu-C produced by this pathogen. It permits localized on-demand delivery of the antimicrobial drug directly at the infectious site.},

note = {2009/25},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN1589,

title = {Temporal multiomic modeling reveals a B-cell receptor proliferative program in chronic lymphocytic leukemia},

author = {C. Schleiss and R. Carapito and L. M. Fornecker and L. Muller and N. Paul and O. Tahar and A. Pichot and M. Tavian and A. Nicolae and L. Miguet and L. Mauvieux and R. Herbrecht and S. Cianferani and J. N. Freund and C. Carapito and M. Maumy-Bertrand and S. Bahram and F. Bertrand and L. Vallat},

url = {https://www.ncbi.nlm.nih.gov/pubmed/33833385},

doi = {10.1038/s41375-021-01221-5},

issn = {1476-5551 (Electronic) 

0887-6924 (Linking)},

year  = {2021},

date = {2021-01-01},

journal = {Leukemia},

volume = {35},

number = {5},

pages = {1463-1474},

abstract = {B-cell receptor (BCR) signaling is crucial for the pathophysiology of most mature B-cell lymphomas/leukemias and has emerged as a therapeutic target whose effectiveness remains limited by the occurrence of mutations. Therefore, deciphering the cellular program activated downstream this pathway has become of paramount importance for the development of innovative therapies. Using an original ex vivo model of BCR-induced proliferation of chronic lymphocytic leukemia cells, we generated 108 temporal transcriptional and proteomic profiles from 1 h up to 4 days after BCR activation. This dataset revealed a structured temporal response composed of 13,065 transcripts and 4027 proteins, comprising a leukemic proliferative signature consisting of 430 genes and 374 proteins. Mathematical modeling of this complex cellular response further highlighted a transcriptional network driven by 14 early genes linked to proteins involved in cell proliferation. This group includes expected genes (EGR1/2, NF-kB) and genes involved in NF-kB signaling modulation (TANK, ROHF) and immune evasion (KMO, IL4I1) that have not yet been associated with leukemic cells proliferation. Our study unveils the BCR-activated proliferative genetic program in primary leukemic cells. This approach combining temporal measurements with modeling allows identifying new putative targets for innovative therapy of lymphoid malignancies and also cancers dependent on ligand-receptor interactions.},

note = {2015/10},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN1675,

title = {Bicyclo[6.1.0]nonyne carboxylic acid for the production of stable molecular probes},

author = {T. Rady and M. Mosser and M. Nothisen and S. Erb and I. Dovgan and S. Cianferani and A. Wagner and G. Chaubet},

url = {<Go to ISI>://WOS:000719362900001},

doi = {10.1039/d1ra07905k},

year  = {2021},

date = {2021-01-01},

journal = {Rsc Advances},

volume = {11},

number = {58},

pages = {36777-36780},

abstract = {Bicyclo[6.1.0]non-4-yn-9-ylmethanol (BCN alcohol) is the most prominent strained-alkyne scaffold in chemical biology. Described herein is the synthesis of an oxidized analogue - BCN acid - whose facile functionalization via amide bond formation yields more stable derivatives than the classically encountered carbamates.},

note = {2021-12},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN1587,

title = {Fast Afucosylation Profiling of Glycoengineered Antibody Subunits by Middle-Up Mass Spectrometry},

author = {E. Wagner-Rousset and O. Colas and S. Chenu and Y. N. Francois and D. Guillarme and S. Cianferani and Y. O. Tsybin and J. Sjogren and A. Delobel and A. Beck},

url = {https://www.ncbi.nlm.nih.gov/pubmed/33908000},

doi = {10.1007/978-1-0716-1241-5_5},

issn = {1940-6029 (Electronic) 

1064-3745 (Linking)},

year  = {2021},

date = {2021-01-01},

journal = {Methods Mol Biol},

volume = {2271},

pages = {73-83},

abstract = {Middle-up LC-MS antibody characterization workflows using reduction or IdeS digestion for a focused assessment of N-glycan profiling of three representative glycoengineered monoclonal antibodies (mAbs), namely, obinutuzumab (GlycomAb technology, Glycart/Roche), benralizumab (Potelligent Technology, BioWa, Kyowa Kirin) and mAb B (kifunensine) and compared to mAb A, produced in a common CHO cell line. In addition, EndoS or EndoS2 enzyme are used for quantitative determination of Fc-glycan core afucosylation and high mannose for these antibodies, as requested by health authorities for Fc-competent therapeutics mAbs critical quality attributes (CQAs).},

note = {pas de projet (chapitre de livre)},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN1602,

title = {Mapping rRNA 2'-O-methylations and identification of C/D snoRNAs in Arabidopsis thaliana plants},

author = {J. Azevedo-Favory and C. Gaspin and L. Ayadi and C. Montacie and V. Marchand and E. Jobet and M. Rompais and C. Carapito and Y. Motorin and J. Saez-Vasquez},

url = {https://www.ncbi.nlm.nih.gov/pubmed/33596769},

doi = {10.1080/15476286.2020.1869892},

issn = {1555-8584 (Electronic) 

1547-6286 (Linking)},

year  = {2021},

date = {2021-01-01},

journal = {RNA Biol},

pages = {1-18},

abstract = {In all eukaryotic cells, the most abundant modification of ribosomal RNA (rRNA) is methylation at the ribose moiety (2'-O-methylation). Ribose methylation at specific rRNA sites is guided by small nucleolar RNAs (snoRNAs) of C/D-box type (C/D snoRNA) and achieved by the methyltransferase Fibrillarin (FIB). Here we used the Illumina-based RiboMethSeq approach for mapping rRNA 2'-O-methylation sites in A. thaliana Col-0 (WT) plants. This analysis detected novel C/D snoRNA-guided rRNA 2'-O-methylation positions and also some orphan sites without a matching C/D snoRNA. Furthermore, immunoprecipitation of Arabidopsis FIB2 identified and demonstrated expression of C/D snoRNAs corresponding to majority of mapped rRNA sites. On the other hand, we show that disruption of Arabidopsis Nucleolin 1 gene (NUC1), encoding a major nucleolar protein, decreases 2'-O-methylation at specific rRNA sites suggesting functional/structural interconnections of 2'-O-methylation with nucleolus organization and plant development. Finally, based on our findings and existent database sets, we introduce a new nomenclature system for C/D snoRNA in Arabidopsis plants.},

note = {2018/13},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN1817,

title = {Strongly Adhesive and Antimicrobial Peptide-Loaded, Alginate–Catechol-Based Gels for Application against Periimplantitis},

author = {S. Baixe and V. Ball and L. Jierry and S. Cianférani and J. -M. Strub and Y. Haikel and M. -H. Metz-Boutigue and O. Etienne},

doi = {doi.org/10.3390/app112110050},

year  = {2021},

date = {2021-01-01},

journal = {Applied Sciences},

volume = {11},

pages = {10050},

note = {2009-25},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN1588,

title = {A structural signature motif enlightens the origin and diversification of nuclear receptors},

author = {B. Beinsteiner and G. V. Markov and S. Erb and Y. Chebaro and A. G. McEwen and S. Cianferani and V. Laudet and D. Moras and I. M. L. Billas},

url = {https://www.ncbi.nlm.nih.gov/pubmed/33882063},

doi = {10.1371/journal.pgen.1009492},

issn = {1553-7404 (Electronic) 

1553-7390 (Linking)},

year  = {2021},

date = {2021-01-01},

journal = {PLoS Genet},

volume = {17},

number = {4},

pages = {e1009492},

abstract = {Nuclear receptors are ligand-activated transcription factors that modulate gene regulatory networks from embryonic development to adult physiology and thus represent major targets for clinical interventions in many diseases. Most nuclear receptors function either as homodimers or as heterodimers. The dimerization is crucial for gene regulation by nuclear receptors, by extending the repertoire of binding sites in the promoters or the enhancers of target genes via combinatorial interactions. Here, we focused our attention on an unusual structural variation of the alpha-helix, called pi-turn that is present in helix H7 of the ligand-binding domain of RXR and HNF4. By tracing back the complex evolutionary history of the pi-turn, we demonstrate that it was present ancestrally and then independently lost in several nuclear receptor lineages. Importantly, the evolutionary history of the pi-turn motif is parallel to the evolutionary diversification of the nuclear receptor dimerization ability from ancestral homodimers to derived heterodimers. We then carried out structural and biophysical analyses, in particular through point mutation studies of key RXR signature residues and showed that this motif plays a critical role in the network of interactions stabilizing homodimers. We further showed that the pi-turn was instrumental in allowing a flexible heterodimeric interface of RXR in order to accommodate multiple interfaces with numerous partners and critical for the emergence of high affinity receptors. Altogether, our work allows to identify a functional role for the pi-turn in oligomerization of nuclear receptors and reveals how this motif is linked to the emergence of a critical biological function. We conclude that the pi-turn can be viewed as a structural exaptation that has contributed to enlarging the functional repertoire of nuclear receptors.},

note = {2020/04},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN1608,

title = {Body Protein Sparing in Hibernators: A Source for Biomedical Innovation},

author = {F. Bertile and C. Habold and Y. Le Maho and S. Giroud},

url = {https://www.ncbi.nlm.nih.gov/pubmed/33679446},

doi = {10.3389/fphys.2021.634953},

issn = {1664-042X (Print) 

1664-042X (Linking)},

year  = {2021},

date = {2021-01-01},

journal = {Front Physiol},

volume = {12},

pages = {634953},

abstract = {Proteins are not only the major structural components of living cells but also ensure essential physiological functions within the organism. Any change in protein abundance and/or structure is at risk for the proper body functioning and/or survival of organisms. Death following starvation is attributed to a loss of about half of total body proteins, and body protein loss induced by muscle disuse is responsible for major metabolic disorders in immobilized patients, and sedentary or elderly people. Basic knowledge of the molecular and cellular mechanisms that control proteostasis is continuously growing. Yet, finding and developing efficient treatments to limit body/muscle protein loss in humans remain a medical challenge, physical exercise and nutritional programs managing to only partially compensate for it. This is notably a major challenge for the treatment of obesity, where therapies should promote fat loss while preserving body proteins. In this context, hibernating species preserve their lean body mass, including muscles, despite total physical inactivity and low energy consumption during torpor, a state of drastic reduction in metabolic rate associated with a more or less pronounced hypothermia. The present review introduces metabolic, physiological, and behavioral adaptations, e.g., energetics, body temperature, and nutrition, of the torpor or hibernation phenotype from small to large mammals. Hibernating strategies could be linked to allometry aspects, the need for periodic rewarming from torpor, and/or the ability of animals to fast for more or less time, thus determining the capacity of individuals to save proteins. Both fat- and food-storing hibernators rely mostly on their body fat reserves during the torpid state, while minimizing body protein utilization. A number of them may also replenish lost proteins during arousals by consuming food. The review takes stock of the physiological, molecular, and cellular mechanisms that promote body protein and muscle sparing during the inactive state of hibernation. Finally, the review outlines how the detailed understanding of these mechanisms at play in various hibernators is expected to provide innovative solutions to fight human muscle atrophy, to better help the management of obese patients, or to improve the ex vivo preservation of organs.},

note = {2011/34},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN1607,

title = {Daytime Restricted Feeding Affects Day-Night Variations in Mouse Cerebellar Proteome},

author = {F. Bertile and M. Plumel and P. Maes and A. Hirschler and E. Challet},

url = {https://www.ncbi.nlm.nih.gov/pubmed/33912010},

doi = {10.3389/fnmol.2021.613161},

issn = {1662-5099 (Print) 

1662-5099 (Linking)},

year  = {2021},

date = {2021-01-01},

journal = {Front Mol Neurosci},

volume = {14},

pages = {613161},

abstract = {The cerebellum harbors a circadian clock that can be shifted by scheduled mealtime and participates in behavioral anticipation of food access. Large-scale two-dimensional difference gel electrophoresis (2D-DIGE) combined with mass spectrometry was used to identify day-night variations in the cerebellar proteome of mice fed either during daytime or nighttime. Experimental conditions led to modified expression of 89 cerebellar proteins contained in 63 protein spots. Five and 33 spots were changed respectively by time-of-day or feeding conditions. Strikingly, several proteins of the heat-shock protein family (i.e., Hsp90aa1, 90ab1, 90b1, and Hspa2, 4, 5, 8, 9) were down-regulated in the cerebellum of daytime food-restricted mice. This was also the case for brain fatty acid protein (Fabp7) and enzymes involved in oxidative phosphorylation (Ndufs1) or folate metabolism (Aldh1l1). In contrast, aldolase C (Aldoc or zebrin II) and pyruvate carboxylase (Pc), two enzymes involved in carbohydrate metabolism, and vesicle-fusing ATPase (Nsf) were up-regulated during daytime restricted feeding, possibly reflecting increased neuronal activity. Significant feeding x time-of-day interactions were found for changes in the intensity of 20 spots. Guanine nucleotide-binding protein G(o) subunit alpha (Gnao1) was more expressed in the cerebellum before food access. Neuronal calcium-sensor proteins [i.e., parvalbumin (Pvalb) and visinin-like protein 1 (Vsnl1)] were inversely regulated in daytime food-restricted mice, compared to control mice fed at night. Furthermore, expression of three enzymes modulating the circadian clockwork, namely heterogeneous nuclear ribonucleoprotein K (Hnrnpk), serine/threonine-protein phosphatases 1 (Ppp1cc and Ppp1cb subunits) and 5 (Ppp5), was differentially altered by daytime restricted feeding. Besides cerebellar proteins affected only by feeding conditions or daily cues, specific changes in in protein abundance before food access may be related to behavioral anticipation of food access and/or feeding-induced shift of the cerebellar clockwork.},

note = {2012/26},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN1591,

title = {Combining label-free and label-based accurate quantifications with SWATH-MS: Comparison with SRM and PRM for the evaluation of bovine muscle type effects},

author = {J. Bons and G. Husson and M. Chion and M. Bonnet and M. Maumy-Bertrand and F. Delalande and S. Cianferani and F. Bertrand and B. Picard and C. Carapito},

url = {https://www.ncbi.nlm.nih.gov/pubmed/33733615},

doi = {10.1002/pmic.202000214},

issn = {1615-9861 (Electronic) 

1615-9853 (Linking)},

year  = {2021},

date = {2021-01-01},

journal = {Proteomics},

volume = {21},

number = {10},

pages = {e2000214},

abstract = {Mass spectrometry has proven to be a valuable tool for the accurate quantification of proteins. In this study, the performances of three targeted approaches, namely selected reaction monitoring (SRM), parallel reaction monitoring (PRM) and sequential windowed acquisition of all theoretical fragment ion mass spectra (SWATH-MS), to accurately quantify ten potential biomarkers of beef meat tenderness or marbling in a cohort of 64 muscle samples were evaluated. So as to get the most benefit out of the complete MS2 maps that are acquired in SWATH-MS, an original label-free quantification method to estimate protein amounts using an I-spline regression model was developed. Overall, SWATH-MS outperformed SRM in terms of sensitivity and dynamic range, while PRM still performed the best, and all three strategies showed similar quantification accuracies and precisions for the absolute quantification of targets of interest. This targeted picture was extended by 585 additional proteins for which amounts were estimated using the label-free approach on SWATH-MS; thus, offering a more global profiling of muscle proteomes and further insights into muscle type effect on candidate biomarkers of beef meat qualities as well as muscle metabolism.},

note = {2017/14},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN1590,

title = {The box C/D snoRNP assembly factor Bcd1 interacts with the histone chaperone Rtt106 and controls its transcription dependent activity},

author = {B. Bragantini and C. Charron and M. Bourguet and A. Paul and D. Tiotiu and B. Rothe and H. Marty and G. Terral and S. Hessmann and L. Decourty and M. E. Chagot and J. M. Strub and S. Massenet and E. Bertrand and M. Quinternet and C. Saveanu and S. Cianferani and S. Labialle and X. Manival and B. Charpentier},

url = {https://www.ncbi.nlm.nih.gov/pubmed/33767140},

doi = {10.1038/s41467-021-22077-4},

issn = {2041-1723 (Electronic) 

2041-1723 (Linking)},

year  = {2021},

date = {2021-01-01},

journal = {Nat Commun},

volume = {12},

number = {1},

pages = {1859},

abstract = {Biogenesis of eukaryotic box C/D small nucleolar ribonucleoproteins initiates co-transcriptionally and requires the action of the assembly machinery including the Hsp90/R2TP complex, the Rsa1p:Hit1p heterodimer and the Bcd1 protein. We present genetic interactions between the Rsa1p-encoding gene and genes involved in chromatin organization including RTT106 that codes for the H3-H4 histone chaperone Rtt106p controlling H3K56ac deposition. We show that Bcd1p binds Rtt106p and controls its transcription-dependent recruitment by reducing its association with RNA polymerase II, modulating H3K56ac levels at gene body. We reveal the 3D structures of the free and Rtt106p-bound forms of Bcd1p using nuclear magnetic resonance and X-ray crystallography. The interaction is also studied by a combination of biophysical and proteomic techniques. Bcd1p interacts with a region that is distinct from the interaction interface between the histone chaperone and histone H3. Our results are evidence for a protein interaction interface for Rtt106p that controls its transcription-associated activity.},

note = {2008/37},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN1615,

title = {A Class of Valuable (Pro-)Activity-Based Protein Profiling Probes: Application to the Redox-Active Antiplasmodial Agent, Plasmodione},

author = {B. A. Cichocki and V. Khobragade and M. Donzel and L. Cotos and S. Blandin and C. Schaeffer-Reiss and S. Cianferani and J. M. Strub and M. Elhabiri and E. Davioud-Charvet},

url = {https://www.ncbi.nlm.nih.gov/pubmed/34056636},

doi = {10.1021/jacsau.1c00025},

issn = {2691-3704 (Electronic) 

2691-3704 (Linking)},

year  = {2021},

date = {2021-01-01},

journal = {JACS Au},

volume = {1},

number = {5},

pages = {669-689},

abstract = {Plasmodione (PD) is a potent antimalarial redox-active drug acting at low nM range concentrations on different malaria parasite stages. In this study, in order to determine the precise PD protein interactome in parasites, we developed a class of (pro-)activity-based protein profiling probes (ABPP) as precursors of photoreactive benzophenone-like probes based on the skeleton of PD metabolites (PDO) generated in a cascade of redox reactions. Under UV-photoirradiation, we clearly demonstrate that benzylic oxidation of 3-benzylmenadione 11 produces the 3-benzoylmenadione probe 7, allowing investigation of the proof-of-concept of the ABPP strategy with 3-benzoylmenadiones 7-10. The synthesized 3-benzoylmenadiones, probe 7 with an alkyne group or probe 9 with -NO2 in para position of the benzoyl chain, were found to be the most efficient photoreactive and clickable probes. In the presence of various H-donor partners, the UV-irradiation of the photoreactive ABPP probes generates different adducts, the expected "benzophenone-like" adducts (pathway 1) in addition to "benzoxanthone" adducts (via two other pathways, 2 and 3). Using both human and Plasmodium falciparum glutathione reductases, three protein ligand binding sites were identified following photolabeling with probes 7 or 9. The photoreduction of 3-benzoylmenadiones (PDO and probe 9) promoting the formation of both the corresponding benzoxanthone and the derived enone could be replaced by the glutathione reductase-catalyzed reduction step. In particular, the electrophilic character of the benzoxanthone was evidenced by its ability to alkylate heme, as a relevant event supporting the antimalarial mode of action of PD. This work provides a proof-of-principle that (pro-)ABPP probes can generate benzophenone-like metabolites enabling optimized activity-based protein profiling conditions that will be instrumental to analyze the interactome of early lead antiplasmodial 3-benzylmenadiones displaying an original and innovative mode of action.},

note = {2019/17},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN1651,

title = {Concurrent BMP Signaling Maintenance and TGF-beta Signaling Inhibition Is a Hallmark of Natural Resistance to Muscle Atrophy in the Hibernating Bear},

author = {L. Cussonneau and C. Boyer and C. Brun and C. Deval and E. Loizon and E. Meugnier and E. Gueret and E. Dubois and D. Taillandier and C. Polge and D. Bechet and G. Gauquelin-Koch and A. L. Evans and J. M. Arnemo and J. E. Swenson and S. Blanc and C. Simon and E. Lefai and F. Bertile and L. Combaret},

url = {https://www.ncbi.nlm.nih.gov/pubmed/34440643},

doi = {10.3390/cells10081873},

issn = {2073-4409 (Electronic) 

2073-4409 (Linking)},

year  = {2021},

date = {2021-01-01},

journal = {Cells},

volume = {10},

number = {8},

abstract = {Muscle atrophy arises from a multiplicity of physio-pathological situations and has very detrimental consequences for the whole body. Although knowledge of muscle atrophy mechanisms keeps growing, there is still no proven treatment to date. This study aimed at identifying new drivers for muscle atrophy resistance. We selected an innovative approach that compares muscle transcriptome between an original model of natural resistance to muscle atrophy, the hibernating brown bear, and a classical model of induced atrophy, the unloaded mouse. Using RNA sequencing, we identified 4415 differentially expressed genes, including 1746 up- and 2369 down-regulated genes, in bear muscles between the active versus hibernating period. We focused on the Transforming Growth Factor (TGF)-beta and the Bone Morphogenetic Protein (BMP) pathways, respectively, involved in muscle mass loss and maintenance. TGF-beta- and BMP-related genes were overall down- and up-regulated in the non-atrophied muscles of the hibernating bear, respectively, and the opposite occurred for the atrophied muscles of the unloaded mouse. This was further substantiated at the protein level. Our data suggest TGF-beta/BMP balance is crucial for muscle mass maintenance during long-term physical inactivity in the hibernating bear. Thus, concurrent activation of the BMP pathway may potentiate TGF-beta inhibiting therapies already targeted to prevent muscle atrophy.},

note = {2011/34},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN1593,

title = {A proteomic view of cellular responses of macrophages to copper when added as ion or as copper-polyacrylate complex},

author = {B. Dalzon and J. Devcic and J. Bons and A. Torres and H. Diemer and S. Ravanel and V. Collin-Faure and S. Cianferani and C. Carapito and T. Rabilloud},

url = {https://www.ncbi.nlm.nih.gov/pubmed/33662612},

doi = {10.1016/j.jprot.2021.104178},

issn = {1876-7737 (Electronic) 

1874-3919 (Linking)},

year  = {2021},

date = {2021-01-01},

journal = {J Proteomics},

volume = {239},

pages = {104178},

abstract = {Copper is an essential metal for life, but is toxic at high concentrations. In mammalian cells, two copper transporters are known, CTR1 and CTR2. In order to gain insights on the possible influence of the import pathway on cellular responses to copper, two copper challenges were compared: one with copper ion, which is likely to use preferentially CTR1, and one with a copper-polyacrylate complex, which will be internalized via the endosomal pathway and is likely to use preferentially CTR2. A model system consisting in the J774A1 mouse macrophage system, with a strong endosomal/lysosomal pathway, was used. In order to gain wide insights into the cellular responses to copper, a proteomic approach was used. The proteomic results were validated by targeted experiments, and showed differential effects of the import mode on cellular physiology parameters. While the mitochondrial transmembrane potential was kept constant, a depletion in the free glutahione content was observed with copper (ion and polylacrylate complex). Both copper-polyacrylate and polyacrylate induced perturbations in the cytoskeleton and in phagocytosis. Inflammatory responses were also differently altered by copper ion and copper-polyacrylate. Copper-polyacrylate also perturbed several metabolic enzymes. Lastly, enzymes were used as a test set to assess the predictive value of proteomics. SIGNIFICANCE: Proteomic profiling provides an in depth analysis of the alterations induced on cells by copper under two different exposure modes to this metal, namely as the free ion or as a complex with polyacrylate. The cellular responses were substantially different between the two exposure modes, although some cellular effects are shared, such as the depletion in free glutathione. Targeted experiments were used to confirm the proteomic results. Some metabolic enzymes showed altered activities after exposure to the copper-polyacrylate complex. The basal inflammatory responses were different for copper ion and for the copper-polyacrylate complex, while the two forms of copper inhibited lipopolysaccharide-induced inflammatory responses.},

note = {2014/29},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN1595,

title = {Rab7-harboring vesicles are carriers of the transferrin receptor through the biosynthetic secretory pathway},

author = {M. S. Deffieu and I. Cesonyte and F. Delalande and G. Boncompain and C. Dorobantu and E. Song and V. Lucansky and A. Hirschler and S. Cianferani and F. Perez and C. Carapito and R. Gaudin},

url = {https://www.ncbi.nlm.nih.gov/pubmed/33523982},

doi = {10.1126/sciadv.aba7803},

issn = {2375-2548 (Electronic) 

2375-2548 (Linking)},

year  = {2021},

date = {2021-01-01},

journal = {Sci Adv},

volume = {7},

number = {2},

abstract = {The biosynthetic secretory pathway is particularly challenging to investigate as it is underrepresented compared to the abundance of the other intracellular trafficking routes. Here, we combined the retention using selective hook (RUSH) to a CRISPR-Cas9 gene editing approach (eRUSH) and identified Rab7-harboring vesicles as an important intermediate compartment of the Golgi-to-plasma membrane transport of neosynthesized transferrin receptor (TfR). These vesicles did not exhibit degradative properties and were not associated to Rab6A-harboring vesicles. Rab7A was transiently associated to neosynthetic TfR-containing post-Golgi vesicles but dissociated before fusion with the plasma membrane. Together, our study reveals a role for Rab7 in the biosynthetic secretory pathway of the TfR, highlighting the diversity of the secretory vesicles' nature.},

note = {2020/15},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN1596,

title = {Mechanistic insights into the synergistic activation of the RXR-PXR heterodimer by endocrine disruptor mixtures},

author = {V. Delfosse and T. Huet and D. Harrus and M. Granell and M. Bourguet and C. Gardia-Parege and B. Chiavarina and M. Grimaldi and S. Le Mevel and P. Blanc and D. Huang and J. Gruszczyk and B. Demeneix and S. Cianferani and J. B. Fini and P. Balaguer and W. Bourguet},

url = {https://www.ncbi.nlm.nih.gov/pubmed/33361153},

doi = {10.1073/pnas.2020551118},

issn = {1091-6490 (Electronic) 

0027-8424 (Linking)},

year  = {2021},

date = {2021-01-01},

journal = {Proc Natl Acad Sci U S A},

volume = {118},

number = {1},

abstract = {Humans are chronically exposed to mixtures of xenobiotics referred to as endocrine-disrupting chemicals (EDCs). A vast body of literature links exposure to these chemicals with increased incidences of reproductive, metabolic, or neurological disorders. Moreover, recent data demonstrate that, when used in combination, chemicals have outcomes that cannot be predicted from their individual behavior. In its heterodimeric form with the retinoid X receptor (RXR), the pregnane X receptor (PXR) plays an essential role in controlling the mammalian xenobiotic response and mediates both beneficial and detrimental effects. Our previous work shed light on a mechanism by which a binary mixture of xenobiotics activates PXR in a synergistic fashion. Structural analysis revealed that mutual stabilization of the compounds within the ligand-binding pocket of PXR accounts for the enhancement of their binding affinity. In order to identify and characterize additional active mixtures, we combined a set of cell-based, biophysical, structural, and in vivo approaches. Our study reveals features that confirm the binding promiscuity of this receptor and its ability to accommodate bipartite ligands. We reveal previously unidentified binding mechanisms involving dynamic structural transitions and covalent coupling and report four binary mixtures eliciting graded synergistic activities. Last, we demonstrate that the robust activity obtained with two synergizing PXR ligands can be enhanced further in the presence of RXR environmental ligands. Our study reveals insights as to how low-dose EDC mixtures may alter physiology through interaction with RXR-PXR and potentially several other nuclear receptor heterodimers.},

note = {2019/06},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN1611,

title = {High-Resolution IMS-MS to Assign Additional Disulfide Bridge Pairing in Complementarity-Determining Regions of an IgG4 Monoclonal Antibody},

author = {E. Desligniere and T. Botzanowski and H. Diemer and D. A. Cooper-Shepherd and E. Wagner-Rousset and O. Colas and G. Bechade and K. Giles and O. Hernandez-Alba and A. Beck and S. Cianferani},

url = {https://www.ncbi.nlm.nih.gov/pubmed/34437803},

doi = {10.1021/jasms.1c00151},

issn = {1879-1123 (Electronic) 

1044-0305 (Linking)},

year  = {2021},

date = {2021-01-01},

journal = {J Am Soc Mass Spectrom},

volume = {32},

number = {10},

pages = {2505-2512},

abstract = {Monoclonal antibodies (mAbs) have taken on an increasing importance for the treatment of various diseases, including cancers and immunological disorders. Disulfide bonds play a pivotal role in therapeutic antibody structure and activity relationships. Disulfide connectivity and cysteine-related variants are considered as critical quality attributes that must be monitored during mAb manufacturing and storage, as non-native disulfide bridges and aggregates might be responsible for loss of biological function and immunogenicity. The presence of cysteine residues in the complementarity-determining regions (CDRs) is rare in human antibodies but may be critical for the antigen-binding or deleterious for therapeutic antibody development. Consequently, in-depth characterization of their disulfide network is a prerequisite for mAb developability assessment. Mass spectrometry (MS) techniques represent powerful tools for accurate identification of disulfide connectivity. We report here on the MS-based characterization of an IgG4 comprising two additional cysteine residues in the CDR of its light chain. Classical bottom-up approaches after trypsin digestion first allowed identification of a dipeptide containing two disulfide bridges. To further investigate the conformational heterogeneity of the disulfide-bridged dipeptide, we performed ion mobility spectrometry-mass spectrometry (IMS-MS) experiments. Our results highlight benefits of high resolution IMS-MS to tackle the conformational landscape of disulfide peptides generated after trypsin digestion of a humanized IgG4 mAb under development. By comparing arrival time distributions of the mAb-collected and synthetic peptides, cyclic IMS afforded unambiguous assessment of disulfide bonds. In addition to classical peptide mapping, qualitative high-resolution IMS-MS can be of great interest to identify disulfide bonds within therapeutic mAbs.},

note = {2016/06},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN1614,

title = {State-of-the-Art Native Mass Spectrometry and Ion Mobility Methods to Monitor Homogeneous Site-Specific Antibody-Drug Conjugates Synthesis},

author = {E. Desligniere and A. Ehkirch and B. L. Duivelshof and H. Toftevall and J. Sjogren and D. Guillarme and V. D'Atri and A. Beck and O. Hernandez-Alba and S. Cianferani},

url = {https://www.ncbi.nlm.nih.gov/pubmed/34073805},

doi = {10.3390/ph14060498},

issn = {1424-8247 (Print) 

1424-8247 (Linking)},

year  = {2021},

date = {2021-01-01},

journal = {Pharmaceuticals (Basel)},

volume = {14},

number = {6},

abstract = {Antibody-drug conjugates (ADCs) are biotherapeutics consisting of a tumor-targeting monoclonal antibody (mAb) linked covalently to a cytotoxic drug. Early generation ADCs were predominantly obtained through non-selective conjugation methods based on lysine and cysteine residues, resulting in heterogeneous populations with varying drug-to-antibody ratios (DAR). Site-specific conjugation is one of the current challenges in ADC development, allowing for controlled conjugation and production of homogeneous ADCs. We report here the characterization of a site-specific DAR2 ADC generated with the GlyCLICK three-step process, which involves glycan-based enzymatic remodeling and click chemistry, using state-of-the-art native mass spectrometry (nMS) methods. The conjugation process was monitored with size exclusion chromatography coupled to nMS (SEC-nMS), which offered a straightforward identification and quantification of all reaction products, providing a direct snapshot of the ADC homogeneity. Benefits of SEC-nMS were further demonstrated for forced degradation studies, for which fragments generated upon thermal stress were clearly identified, with no deconjugation of the drug linker observed for the T-GlyGLICK-DM1 ADC. Lastly, innovative ion mobility-based collision-induced unfolding (CIU) approaches were used to assess the gas-phase behavior of compounds along the conjugation process, highlighting an increased resistance of the mAb against gas-phase unfolding upon drug conjugation. Altogether, these state-of-the-art nMS methods represent innovative approaches to investigate drug loading and distribution of last generation ADCs, their evolution during the bioconjugation process and their impact on gas-phase stabilities. We envision nMS and CIU methods to improve the conformational characterization of next generation-empowered mAb-derived products such as engineered nanobodies, bispecific ADCs or immunocytokines.},

note = {2018/28},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN1676,

title = {Pushing the limits of native MS: Online SEC-native MS for structural biology applications},

author = {E. Desligniere and M. Ley and M. Bourguet and A. Ehkirch and T. Botzanowski and S. Erb and O. Hernandez-Alba and S. Cianferani},

url = {<Go to ISI>://WOS:000616138200011},

doi = {ARTN 116502 

10.1016/j.ijms.2020.116502},

issn = {1387-3806},

year  = {2021},

date = {2021-01-01},

journal = {International Journal of Mass Spectrometry},

volume = {461},

abstract = {Native mass spectrometry (nMS) is now widely applied to investigate non-covalently assembled biomolecule complexes. nMS requires the use of near-neutral pH and volatile buffers to preserve the native state of proteins. However, buffer exchange into nMS-compatible solvent is usually performed manually, which results in a time-consuming and tedious process, thus appearing as a major drawback for nMS analysis. Conversely, online coupling of size exclusion chromatography (SEC) to nMS affords a fast-automated and improved desalting, but also provides an additional dimension of separation for complex protein mixtures. We illustrate here the benefits of SEC-nMS compared to manual offline desalting for the characterization of a wide variety of biological systems, ranging from multiprotein assemblies, protein-ligand and protein-nucleic acid complexes, to proteins in a detergent environment. We then highlight the potential of the coupling to further integrate ion mobility while preserving the native conformations of proteins, allowing for rapid collision cross section measurement and even collision-induced unfolding experiments. Finally, we show that online SEC coupling can also serve as the basis for multidimensional non-denaturing liquid chromatography (LC) workflows, with the SEC acting as a fast desalting device, helping to achieve first dimension LC separation in optimal chromatographic conditions while being compatible with further nMS analysis. (C) 2020 Elsevier B.V. All rights reserved.},

note = {Review 

pas de projet spécifique},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN1597,

title = {Hands on Native Mass Spectrometry Analysis of Multi-protein Complexes},

author = {S. Erb and S. Cianferani and J. Marcoux},

url = {https://www.ncbi.nlm.nih.gov/pubmed/33301118},

doi = {10.1007/978-1-0716-1126-5_10},

issn = {1940-6029 (Electronic) 

1064-3745 (Linking)},

year  = {2021},

date = {2021-01-01},

journal = {Methods Mol Biol},

volume = {2247},

pages = {173-191},

abstract = {By maintaining intact multi-protein complexes in the gas-phase, native mass spectrometry provides their molecular weight with very good accuracy compared to other methods (typically native PAGE or SEC-MALS) (Marcoux and Robinson, Structure 21:1541-1550, 2013). Besides, heterogeneous samples, in terms of both oligomeric states and ligand-bound species can be fully characterized. Here we thoroughly describe the analysis of several oligomeric protein complexes ranging from a 16 = kDa dimer to a 801-kDa tetradecameric complex on different instrumental setups.},

note = {chapitre de livre},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN1604,

title = {Ral GTPases promote breast cancer metastasis by controlling biogenesis and organ targeting of exosomes},

author = {S. Ghoroghi and B. Mary and A. Larnicol and N. Asokan and A. Klein and N. Osmani and I. Busnelli and F. Delalande and N. Paul and S. Halary and F. Gros and L. Fouillen and A. M. Haeberle and C. Royer and C. Spiegelhalter and G. Andre-Gregoire and V. Mittelheisser and A. Detappe and K. Murphy and P. Timpson and R. Carapito and M. Blot-Chabaud and J. Gavard and C. Carapito and N. Vitale and O. Lefebvre and J. G. Goetz and V. Hyenne},

url = {https://www.ncbi.nlm.nih.gov/pubmed/33404012},

doi = {10.7554/eLife.61539},

issn = {2050-084X (Electronic) 

2050-084X (Linking)},

year  = {2021},

date = {2021-01-01},

journal = {Elife},

volume = {10},

abstract = {Cancer extracellular vesicles (EVs) shuttle at distance and fertilize pre-metastatic niches facilitating subsequent seeding by tumor cells. However, the link between EV secretion mechanisms and their capacity to form pre-metastatic niches remains obscure. Using mouse models, we show that GTPases of the Ral family control, through the phospholipase D1, multi-vesicular bodies homeostasis and tune the biogenesis and secretion of pro-metastatic EVs. Importantly, EVs from RalA or RalB depleted cells have limited organotropic capacities in vivoand are less efficient in promoting metastasis. RalA and RalB reduce the EV levels of the adhesion molecule MCAM/CD146, which favors EV-mediated metastasis by allowing EVs targeting to the lungs. Finally, RalA, RalB, and MCAM/CD146, are factors of poor prognosis in breast cancer patients. Altogether, our study identifies RalGTPases as central molecules linking the mechanisms of EVs secretion and cargo loading to their capacity to disseminate and induce pre-metastatic niches in a CD146-dependent manner.},

note = {2019/08},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN1650,

title = {Hibernating brown bears are protected against atherogenic dyslipidemia},

author = {S. Giroud and I. Chery and M. Arrive and M. Prost and J. Zumsteg and D. Heintz and A. L. Evans and G. Gauquelin-Koch and J. M. Arnemo and J. E. Swenson and E. Lefai and F. Bertile and C. Simon and S. Blanc},

url = {https://www.ncbi.nlm.nih.gov/pubmed/34548543},

doi = {10.1038/s41598-021-98085-7},

issn = {2045-2322 (Electronic) 

2045-2322 (Linking)},

year  = {2021},

date = {2021-01-01},

journal = {Sci Rep},

volume = {11},

number = {1},

pages = {18723},

abstract = {To investigate mechanisms by which hibernators avoid atherogenic hyperlipidemia during hibernation, we assessed lipoprotein and cholesterol metabolisms of free-ranging Scandinavian brown bears (Ursus arctos). In winter- and summer-captured bears, we measured lipoprotein sizes and sub-classes, triglyceride-related plasma-enzyme activities, and muscle lipid composition along with plasma-levels of antioxidant capacities and inflammatory markers. Although hibernating bears increased nearly all lipid levels, a 36%-higher cholesteryl-ester transfer-protein activity allowed to stabilize lipid composition of high-density lipoproteins (HDL). Levels of inflammatory metabolites, i.e., 7-ketocholesterol and 11ss-prostaglandin F2alpha, declined in winter and correlated inversely with cardioprotective HDL2b-proportions and HDL-sizes that increased during hibernation. Lower muscle-cholesterol concentrations and lecithin-cholesterol acyltransferase activity in winter suggest that hibernating bears tightly controlled peripheral-cholesterol synthesis and/or release. Finally, greater plasma-antioxidant capacities prevented excessive lipid-specific oxidative damages in plasma and muscles of hibernating bears. Hence, the brown bear manages large lipid fluxes during hibernation, without developing adverse atherogenic effects that occur in humans and non-hibernators.},

note = {211/34},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN1652,

title = {Cardiomyocyte Protection by Hibernating Brown Bear Serum: Toward the Identification of New Protective Molecules Against Myocardial Infarction},

author = {L. Givre and C. Crola Da Silva and J. E. Swenson and J. M. Arnemo and G. Gauquelin-Koch and F. Bertile and E. Lefai and L. Gomez},

url = {https://www.ncbi.nlm.nih.gov/pubmed/34336951},

doi = {10.3389/fcvm.2021.687501},

issn = {2297-055X (Print) 

2297-055X (Linking)},

year  = {2021},

date = {2021-01-01},

journal = {Front Cardiovasc Med},

volume = {8},

pages = {687501},

abstract = {Ischemic heart disease remains one of the leading causes of death worldwide. Despite intensive research on the treatment of acute myocardial infarction, no effective therapy has shown clinical success. Therefore, novel therapeutic strategies are required to protect the heart from reperfusion injury. Interestingly, despite physical inactivity during hibernation, brown bears (Ursus arctos) cope with cardiovascular physiological conditions that would be detrimental to humans. We hypothesized that bear serum might contain circulating factors that could provide protection against cell injury. In this study, we sought to determine whether addition of bear serum might improve cardiomyocyte survival following hypoxia-reoxygenation. Isolated mouse cardiomyocytes underwent 45 min of hypoxia followed by reoxygenation. At the onset of reoxygenation, cells received fetal bovine serum (FBS; positive control), summer (SBS) or winter bear serum (WBS), or adult serums of other species, as indicated. After 2 h of reoxygenation, propidium iodide staining was used to evaluate cell viability by flow cytometry. Whereas, 0.5% SBS tended to decrease reperfusion injury, 0.5% WBS significantly reduced cell death, averaging 74.04 +/- 7.06% vs. 79.20 +/- 6.53% in the FBS group. This cardioprotective effect was lost at 0.1%, became toxic above 5%, and was specific to the bear. Our results showed that bear serum exerts a therapeutic effect with an efficacy threshold, an optimal dose, and a toxic effect on cardiomyocyte viability after hypoxia-reoxygenation. Therefore, the bear serum may be a potential source for identifying new therapeutic molecules to fight against myocardial reperfusion injury and cell death in general.},

note = {2011/34},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN1641,

title = {Biodesulfurization Induces Reprogramming of Sulfur Metabolism in Rhodococcus qingshengii IGTS8: Proteomics and Untargeted Metabolomics},

author = {A. Hirschler and C. Carapito and L. Maurer and J. Zumsteg and C. Villette and D. Heintz and C. Dahl and A. Al-Nayal and V. Sangal and H. Mahmoud and A. Van Dorsselaer and W. Ismail},

url = {https://www.ncbi.nlm.nih.gov/pubmed/34468196},

doi = {10.1128/Spectrum.00692-21},

issn = {2165-0497 (Electronic) 

2165-0497 (Linking)},

year  = {2021},

date = {2021-01-01},

journal = {Microbiol Spectr},

pages = {e0069221},

abstract = {Sulfur metabolism in fuel-biodesulfurizing bacteria and the underlying physiological adaptations are not understood, which has impeded the development of a commercially viable bioprocess for fuel desulfurization. To fill these knowledge gaps, we performed comparative proteomics and untargeted metabolomics in cultures of the biodesulfurization reference strain Rhodococcus qingshengii IGTS8 grown on either inorganic sulfate or the diesel-borne organosulfur compound dibenzothiophene as a sole sulfur source. Dibenzothiophene significantly altered the biosynthesis of many sulfur metabolism proteins and metabolites in a growth phase-dependent manner, which enabled us to reconstruct the first experimental model for sulfur metabolism in a fuel-biodesulfurizing bacterium. All key pathways related to assimilatory sulfur metabolism were represented in the sulfur proteome, including uptake of the sulfur sources, sulfur acquisition, and assimilatory sulfate reduction, in addition to biosynthesis of key sulfur-containing metabolites such as S-adenosylmethionine, coenzyme A, biotin, thiamin, molybdenum cofactor, mycothiol, and ergothioneine (low-molecular weight thiols). Fifty-two proteins exhibited significantly different abundance during at least one growth phase. Sixteen proteins were uniquely detected and 47 proteins were significantly more abundant in the dibenzothiophene culture during at least one growth phase. The sulfate-free dibenzothiophene-containing culture reacted to sulfate starvation by restricting sulfur assimilation, enforcing sulfur-sparing, and maintaining redox homeostasis. Biodesulfurization triggered alternative pathways for sulfur assimilation different from those operating in the inorganic sulfate culture. Sulfur metabolism reprogramming and metabolic switches in the dibenzothiophene culture were manifested in limiting sulfite reduction and biosynthesis of cysteine, while boosting the production of methionine via the cobalamin-independent pathway, as well as the biosynthesis of the redox buffers mycothiol and ergothioneine. The omics data underscore the key role of sulfur metabolism in shaping the biodesulfurization phenotype and highlight potential targets for improving the biodesulfurization catalytic activity via metabolic engineering. IMPORTANCE For many decades, research on biodesulfurization of fossil fuels was conducted amid a large gap in knowledge of sulfur metabolism and its regulation in fuel-biodesulfurizing bacteria, which has impeded the development of a commercially viable bioprocess. In addition, lack of understanding of biodesulfurization-associated metabolic and physiological adaptations prohibited the development of efficient biodesulfurizers. Our integrated omics-based findings reveal the assimilatory sulfur metabolism in the biodesulfurization reference strain Rhodococcus qingshengii IGTS8 and show how sulfur metabolism and oxidative stress response were remodeled and orchestrated to shape the biodesulfurization phenotype. Our findings not only explain the frequently encountered low catalytic activity of native fuel-biodesulfurizing bacteria but also uncover unprecedented potential targets in sulfur metabolism that could be exploited via metabolic engineering to boost the biodesulfurization catalytic activity, a prerequisite for commercial application.},

note = {2017/28},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Zhai2020,

title = {Opposing regulatory functions of the TIM3 (HAVCR2) signalosome in primary effector T cells as revealed by quantitative interactomics.},

author = {Yunhao Zhai and Javier Celis-Gutierrez and Guillaume Voisinne and Daiki Mori and Laura Girard and Odile Burlet-Schiltz and Anne Gonzalez Peredo and Romain Roncagalli and Bernard Malissen},

doi = {10.1038/s41423-020-00575-7},

year  = {2020},

date = {2020-11-01},

journal = {Cellular & molecular immunology},

address = {China},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Eren2020,

title = {Irgm2 and Gate-16 cooperatively dampen Gram-negative bacteria-induced caspase-11 response.},

author = {Elif Eren and Rémi Planès and Salimata Bagayoko and Pierre-Jean Bordignon and Karima Chaoui and Audrey Hessel and Karin Santoni and Miriam Pinilla and Brice Lagrange and Odile Burlet-Schiltz and Jonathan C Howard and Thomas Henry and Masahiro Yamamoto and Etienne Meunier},

doi = {10.15252/embr.202050829},

year  = {2020},

date = {2020-11-01},

journal = {EMBO reports},

volume = {21},

number = {11},

pages = {e50829},

abstract = {Inflammatory caspase-11 (rodent) and caspases-4/5 (humans) detect the Gram-negative bacterial component LPS within the host cell cytosol, promoting activation of the non-canonical inflammasome. Although non-canonical inflammasome-induced pyroptosis and IL-1-related cytokine release are crucial to mount an efficient immune response against various bacteria, their unrestrained activation drives sepsis. This suggests that cellular components tightly control the threshold level of the non-canonical inflammasome in order to ensure efficient but non-deleterious inflammatory responses. Here, we show that the IFN-inducible protein Irgm2 and the ATG8 family member Gate-16 cooperatively counteract Gram-negative bacteria-induced non-canonical inflammasome activation, both in cultured macrophages and in vivo. Specifically, the Irgm2/Gate-16 axis dampens caspase-11 targeting to intracellular bacteria, which lowers caspase-11-mediated pyroptosis and cytokine release. Deficiency in Irgm2 or Gate16 induces both guanylate binding protein (GBP)-dependent and GBP-independent routes for caspase-11 targeting to intracellular bacteria. Our findings identify molecular effectors that fine-tune bacteria-activated non-canonical inflammasome responses and shed light on the understanding of the immune pathways they control.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Klein2020,

title = {Connectivity mapping of glomerular proteins identifies dimethylaminoparthenolide as a new inhibitor of diabetic kidney disease.},

author = {Julie Klein and Cécile Caubet and Mylène Camus and Manousos Makridakis and Colette Denis and Marion Gilet and Guylène Feuillet and Simon Rascalou and Eric Neau and Luc Garrigues and Olivier Boullay and Harald Mischak and Bernard Monsarrat and Odile Burlet-Schiltz and Antonia Vlahou and Jean Sébastien Saulnier-Blache and Jean-Loup Bascands and Joost P Schanstra},

doi = {10.1038/s41598-020-71950-7},

year  = {2020},

date = {2020-09-01},

journal = {Scientific reports},

volume = {10},

number = {1},

pages = {14898},

abstract = {While blocking the renin angiotensin aldosterone system (RAAS) has been the main therapeutic strategy to control diabetic kidney disease (DKD) for many years, 25-30% of diabetic patients still develop the disease. In the present work we adopted a systems biology strategy to analyze glomerular protein signatures to identify drugs with potential therapeutic properties in DKD acting through a RAAS-independent mechanism. Glomeruli were isolated from wild type and type 1 diabetic (Ins2Akita) mice treated or not with the angiotensin-converting enzyme inhibitor (ACEi) ramipril. Ramipril efficiently reduced the urinary albumin/creatine ratio (ACR) of Ins2Akita mice without modifying DKD-associated renal-injuries. Large scale quantitative proteomics was used to identify the DKD-associated glomerular proteins (DKD-GPs) that were ramipril-insensitive (RI-DKD-GPs). The raw data are publicly available via ProteomeXchange with identifier PXD018728. We then applied an in silico drug repurposing approach using a pattern-matching algorithm (Connectivity Mapping) to compare the RI-DKD-GPs's signature with a collection of thousands of transcriptional signatures of bioactive compounds. The sesquiterpene lactone parthenolide was identified as one of the top compounds predicted to reverse the RI-DKD-GPs's signature. Oral treatment of 2 months old Ins2Akita mice with dimethylaminoparthenolide (DMAPT, a water-soluble analogue of parthenolide) for two months at 10 mg/kg/d by gavage significantly reduced urinary ACR. However, in contrast to ramipril, DMAPT also significantly reduced glomerulosclerosis and tubulointerstitial fibrosis. Using a system biology approach, we identified DMAPT, as a compound with a potential add-on value to standard-of-care ACEi-treatment in DKD.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid32096818,

title = {Proline: an efficient and user-friendly software suite for large-scale proteomics},

author = {D Bouyssié and A M Hesse and E Mouton-Barbosa and M Rompais and C Macron and C Carapito and A G Peredo and Y Couté and V Dupierris and A Burel and J P Menetrey and A Kalaitzakis and J Poisat and A Romdhani and O Burlet-Schiltz and S Cianférani and J Garin and C Bruley},

doi = {10.1093/bioinformatics/btaa118},

year  = {2020},

date = {2020-05-01},

journal = {Bioinformatics},

volume = {36},

number = {10},

pages = {3148-3155},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid31911241,

title = {Characterization of Macrophage Galactose-type Lectin (MGL) ligands in colorectal cancer cell lines},

author = {M Pirro and Y Rombouts and A Stella and O Neyrolles and O Burlet-Schiltz and S J Vliet and A H Ru and Y Mohammed and M Wuhrer and P A Veelen and P J Hensbergen},

doi = {10.1016/j.bbagen.2020.129513},

year  = {2020},

date = {2020-04-03},

journal = {Biochim Biophys Acta Gen Subj},

volume = {1864},

number = {4},

pages = {129513},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Locard-Paulet2020a,

title = {Comparing 22 Popular Phosphoproteomics Pipelines for Peptide Identification and Site Localization.},

author = {Marie Locard-Paulet and David Bouyssié and Carine Froment and Odile Burlet-Schiltz and Lars J Jensen},

doi = {10.1021/acs.jproteome.9b00679},

year  = {2020},

date = {2020-03-01},

journal = {Journal of proteome research},

volume = {19},

number = {3},

pages = {1338--1345},

address = {United States},

abstract = {Phosphorylation-driven cell signaling governs most biological functions and is widely studied using mass-spectrometry-based phosphoproteomics. Identifying the peptides and localizing the phosphorylation sites within them from the raw data is challenging and can be performed by several algorithms that return scores that are not directly comparable. This increases the heterogeneity among published phosphoproteomics data sets and prevents their direct integration. Here we compare 22 pipelines implemented in the main software tools used for bottom-up phosphoproteomics analysis (MaxQuant, Proteome Discoverer, PeptideShaker). We test six search engines (Andromeda, Comet, Mascot, MS Amanda, SequestHT, and X!Tandem) in combination with several localization scoring algorithms (delta score, D-score, PTM-score, phosphoRS, and Ascore). We show that these follow very different score distributions, which can lead to different false localization rates for the same threshold. We provide a strategy to discriminate correctly from incorrectly localized phosphorylation sites in a consistent manner across the tested pipelines. The results presented here can help users choose the most appropriate pipeline and cutoffs for their phosphoproteomics analysis.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{643,

title = {Alterations in rat adipose tissue transcriptome and proteome in response to prolonged fasting},

author = {M Ibrahim and D Ayoub and T Wasselin and A Van Dorsselaer and Y Le Maho and T Raclot and F Bertile},

doi = {10.1515/hsz-2019-0184},

year  = {2020},

date = {2020-02-25},

journal = {Biological Chemistry},

volume = {401},

number = {3},

pages = {389-405},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{641,

title = {Quantification of biomarkers for beef meat qualities using a combination of Parallel Reaction Monitoring- and antibody-based proteomics},

author = {M Bonnet and J Soulat and J Bons and S Leger and L De Koning and C Carapito and B Picard},

doi = {10.1016/j.foodchem.2020.126376},

year  = {2020},

date = {2020-02-10},

journal = {Food Chem},

volume = {317},

pages = {126376.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid31975593,

title = {Comparing 22 Popular Phosphoproteomics Pipelines for Peptide Identification and Site Localization},

author = {M Locard-Paulet and D Bouyssié and C Froment and O Burlet-Schiltz and L J Jensen},

doi = {10.1021/acs.jproteome.9b00679},

year  = {2020},

date = {2020-02-04},

journal = {J. Proteome Res.},

volume = {19},

number = {3},

pages = {1338--1345},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid31974367,

title = {Resistance of melanoma to immune checkpoint inhibitors is overcome by targeting the sphingosine kinase-1},

author = {C Imbert and A Montfort and M Fraisse and E Marcheteau and J Gilhodes and E Martin and F Bertrand and M Marcellin and O Burlet-Schiltz and A G Peredo and V Garcia and S Carpentier and S Tartare-Deckert and P Brousset and P Rochaix and F Puisset and T Filleron and N Meyer and L Lamant and T Levade and B Ségui and N Andrieu-Abadie and C Colacios},

doi = {10.1038/s41467-019-14218-7},

year  = {2020},

date = {2020-01-23},

journal = {Nat Commun},

volume = {11},

number = {1},

pages = {437},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid31626997,

title = {Analysis of 5000 year-old human teeth using optimized large-scale and targeted proteomics approaches for detection of sex-specific peptides},

author = {C Froment and M Hourset and N S?enz-Oyh?r?guy and E Mouton-Barbosa and C Willmann and C Zanolli and R Esclassan and R Donat and C Th?ves and O Burlet-Schiltz and C Mollereau},

doi = {10.1016/j.jprot.2019.103548},

year  = {2020},

date = {2020-01-16},

journal = {J Proteomics},

volume = {211},

pages = {103548},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid31919869,

title = {Adipocyte extracellular vesicles carry enzymes and fatty acids that stimulate mitochondrial metabolism and remodeling in tumor cells},

author = {E Clement and I Lazar and C Attané and L Carrié and S Dauvillier and M Ducoux-Petit and D Estève and T Menneteau and M Moutahir and S Le Gonidec and S Dalle and P Valet and O Burlet-Schiltz and C Muller and L Nieto},

doi = {10.15252/embj.2019102525},

year  = {2020},

date = {2020-01-10},

journal = {EMBO J.},

volume = {39},

number = {3},

pages = {e102525},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Santin2020,

title = {Mitochondrial 4-HNE derived from MAO-A promotes mitoCa(2+) overload in chronic postischemic cardiac remodeling.},

author = {Yohan Santin and Loubina Fazal and Yannis Sainte-Marie and Pierre Sicard and Damien Maggiorani and Florence Tortosa and Yasemin Yücel Yücel and Lise Teyssedre and Jacques Rouquette and Marlene Marcellin and Cécile Vindis and Jean C Shih and Olivier Lairez and Odile Burlet-Schiltz and Angelo Parini and Frank Lezoualc'h and Jeanne Mialet-Perez},

doi = {10.1038/s41418-019-0470-y},

year  = {2020},

date = {2020-01-01},

journal = {Cell death and differentiation},

volume = {27},

number = {6},

pages = {1907--1923},

abstract = {Chronic remodeling postmyocardial infarction consists in various maladaptive changes including interstitial fibrosis, cardiomyocyte death and mitochondrial dysfunction that lead to heart failure (HF). Reactive aldehydes such as 4-hydroxynonenal (4-HNE) are critical mediators of mitochondrial dysfunction but the sources of mitochondrial 4-HNE in cardiac diseases together with its mechanisms of action remain poorly understood. Here, we evaluated whether the mitochondrial enzyme monoamine oxidase-A (MAO-A), which generates H(2)O(2) as a by-product of catecholamine metabolism, is a source of deleterious 4-HNE in HF. We found that MAO-A activation increased mitochondrial ROS and promoted local 4-HNE production inside the mitochondria through cardiolipin peroxidation in primary cardiomyocytes. Deleterious effects of MAO-A/4-HNE on cardiac dysfunction were prevented by activation of mitochondrial aldehyde dehydrogenase 2 (ALDH2), the main enzyme for 4-HNE metabolism. Mechanistically, MAO-A-derived 4-HNE bound to newly identified targets VDAC and MCU to promote ER-mitochondria contact sites and MCU higher-order complex formation. The resulting mitochondrial Ca(2+) accumulation participated in mitochondrial respiratory dysfunction and loss of membrane potential, as shown with the protective effects of the MCU inhibitor, RU360. Most interestingly, these findings were recapitulated in a chronic model of ischemic remodeling where pharmacological or genetic inhibition of MAO-A protected the mice from 4-HNE accumulation, MCU oligomer formation and Ca(2+) overload, thus mitigating ventricular dysfunction. To our knowledge, these are the first evidences linking MAO-A activation to mitoCa(2+) mishandling through local 4-HNE production, contributing to energetic failure and postischemic remodeling.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Froment2020,

title = {Analysis of 5000 year-old human teeth using optimized large-scale and targeted proteomics approaches for detection of sex-specific peptides.},

author = {Carine Froment and Mathilde Hourset and Nancy Sáenz-Oyhéréguy and Emmanuelle Mouton-Barbosa and Claire Willmann and Clément Zanolli and Rémi Esclassan and Richard Donat and Catherine Thèves and Odile Burlet-Schiltz and Catherine Mollereau},

doi = {10.1016/j.jprot.2019.103548},

year  = {2020},

date = {2020-01-01},

journal = {Journal of proteomics},

volume = {211},

pages = {103548},

address = {Netherlands},

abstract = {The study demonstrates the high potential of MS-based proteomics coupled to an iterative database search strategy for the in-depth investigation of ancient proteomes. An efficient targeted PRM MS-based approach, although limited to the detection of a single pair of sex-specific amelogenin peptides, allowed confirming the sex of individuals in ancient dental remains, an essential information for paleoanthropologists facing the issue of sex determination and dimorphism.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{del_corpo_atpme17_2020,

title = {AtPME17 is a functional $backslash$textitArabidopsis thaliana pectin methylesterase regulated by its PRO region that triggers PME activity in the resistance to $backslash$textitBotrytis cinerea},

author = {Daniele Del Corpo and Maria R Fullone and Rossella Miele and Mickaël Lafond and Daniela Pontiggia and Sacha Grisel and Sylvie Kieffer‐Jaquinod and Thierry Giardina and Daniela Bellincampi and Vincenzo Lionetti},

url = {https://onlinelibrary.wiley.com/doi/10.1111/mpp.13002},

doi = {10.1111/mpp.13002},

issn = {1464-6722, 1364-3703},

year  = {2020},

date = {2020-01-01},

journal = {Molecular Plant Pathology},

pages = {mpp.13002},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{farhat_morc-driven_2020,

title = {A MORC-driven transcriptional switch controls Toxoplasma developmental trajectories and sexual commitment},

author = {Dayana C Farhat and Christopher Swale and Céline Dard and Dominique Cannella and Philippe Ortet and Mohamed Barakat and Fabien Sindikubwabo and Lucid Belmudes and Pieter-Jan De Bock and Yohann Couté and Alexandre Bougdour and Mohamed-Ali Hakimi},

url = {http://www.nature.com/articles/s41564-020-0674-4},

doi = {10.1038/s41564-020-0674-4},

issn = {2058-5276},

year  = {2020},

date = {2020-01-01},

journal = {Nature Microbiology},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{di_giovanni_behavior-manipulating_2020,

title = {A behavior-manipulating virus relative as a source of adaptive genes for Drosophila parasitoids},

author = {D Di Giovanni and D Lepetit and B Guinet and B Bennetot and M Boulesteix and Y Couté and O Bouchez and M Ravallec and J Varaldi},

doi = {10.1093/molbev/msaa030},

issn = {1537-1719},

year  = {2020},

date = {2020-01-01},

journal = {Molecular Biology and Evolution},

abstract = {Some species of parasitic wasps have domesticated viral machineries to deliver immunosuppressive factors to their hosts. Up to now, all described cases fall into the Ichneumonoidea superfamily, which only represents around 10% of hymenoptera diversity, raising the question of whether such domestication occurred outside this clade. Furthermore, the biology of the ancestral donor viruses is completely unknown. Since the 1980's, we know that Drosophila parasitoids belonging to the Leptopilina genus, which diverged from the Ichneumonoidea superfamily 225My ago, do produce immuno-suppressive virus-like structure in their reproductive apparatus. However, the viral origin of these structures has been the subject of debate. In this paper, we provide genomic and experimental evidence that those structures do derive from an ancestral virus endogenization event. Interestingly, its close relatives induce a behaviour manipulation in present-day wasps. Thus, we conclude that virus domestication is more prevalent than previously thought and that behaviour manipulation may have been instrumental in the birth of such associations.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{adhikari_high-stringency_2020,

title = {A high-stringency blueprint of the human proteome},

author = {Subash Adhikari and Edouard C Nice and Eric W Deutsch and Lydie Lane and Gilbert S Omenn and Stephen R Pennington and Young-Ki Paik and Christopher M Overall and Fernando J Corrales and Ileana M Cristea and Jennifer E Van Eyk and Mathias Uhlén and Cecilia Lindskog and Daniel W Chan and Amos Bairoch and James C Waddington and Joshua L Justice and Joshua LaBaer and Henry Rodriguez and Fuchu He and Markus Kostrzewa and Peipei Ping and Rebekah L Gundry and Peter Stewart and Sanjeeva Srivastava and Sudhir Srivastava and Fabio C S Nogueira and Gilberto B Domont and Yves Vandenbrouck and Maggie P Y Lam and Sara Wennersten and Juan Antonio Vizcaino and Marc Wilkins and Jochen M Schwenk and Emma Lundberg and Nuno Bandeira and Gyorgy Marko-Varga and Susan T Weintraub and Charles Pineau and Ulrike Kusebauch and Robert L Moritz and Seong Beom Ahn and Magnus Palmblad and Michael P Snyder and Ruedi Aebersold and Mark S Baker},

doi = {10.1038/s41467-020-19045-9},

issn = {2041-1723},

year  = {2020},

date = {2020-01-01},

journal = {Nature Communications},

volume = {11},

number = {1},

pages = {5301},

abstract = {The Human Proteome Organization (HUPO) launched the Human Proteome Project (HPP) in 2010, creating an international framework for global collaboration, data sharing, quality assurance and enhancing accurate annotation of the genome-encoded proteome. During the subsequent decade, the HPP established collaborations, developed guidelines and metrics, and undertook reanalysis of previously deposited community data, continuously increasing the coverage of the human proteome. On the occasion of the HPP's tenth anniversary, we here report a 90.4% complete high-stringency human proteome blueprint. This knowledge is essential for discerning molecular processes in health and disease, as we demonstrate by highlighting potential roles the human proteome plays in our understanding, diagnosis and treatment of cancers, cardiovascular and infectious diseases.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{monestier_liver-targeting_2020,

title = {A liver-targeting Cu( textlessspan style=},

author = {Marie Monestier and Anaïs M Pujol and Aline Lamboux and Martine Cuillel and Isabelle Pignot-Paintrand and Doris Cassio and Peggy Charbonnier and Khémary Um and Amélie Harel and Sylvain Bohic and Christelle Gateau and Vincent Balter and Virginie Brun and Pascale Delangle and Elisabeth Mintz},

url = {http://xlink.rsc.org/?DOI=D0MT00069H},

doi = {10.1039/D0MT00069H},

issn = {1756-5901, 1756-591X},

year  = {2020},

date = {2020-01-01},

journal = {Metallomics},

pages = {10.1039.D0MT00069H},

abstract = {A hepatocyte-targeting chelator promotes Cu biliary excretion, hence restoring the physiological Cu detoxification pathway in a murine Wilson's disease model. 

, 

 

Copper chelation is the most commonly used therapeutic strategy nowadays to treat Wilson's disease, a genetic disorder primarily inducing a pathological accumulation of Cu in the liver. The mechanism of action of Chel2, a liver-targeting Cu( 

i 

) chelator known to promote intracellular Cu chelation, was studied in hepatic cells that reconstitute polarized epithelia with functional bile canaliculi, reminiscent of the excretion pathway in the liver. The interplay between Chel2 and Cu localization in these cells was demonstrated through confocal microscopy using a fluorescent derivative and nano X-ray fluorescence. The Cu( 

i 

) bound chelator was found in vesicles potentially excreted in the canaliculi. Moreover, injection of Chel2 either intravenously or subcutaneously to a murine model of Wilson's disease increased excretion of Cu in the faeces, confirming 

in vivo 

biliary excretion. Therefore, Chel2 turns out to be a possible means to collect and excrete hepatic Cu in the faeces, hence restoring the physiological pathway.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{van_gool_analytical_2020,

title = {Analytical techniques for multiplex analysis of protein biomarkers},

author = {Alain Van Gool and Fernado Corrales and Mirjana Čolović and Danijela Krstić and Begona Oliver-Martos and Eva Martínez-Cáceres and Ivone Jakasa and Goran Gajski and Virginie Brun and Kyriacos Kyriacou and Izabela Burzynska-Pedziwiatr and Lucyna Alicja Wozniak and Stephan Nierkens and César Pascual García and Jaroslav Katrlik and Zanka Bojic-Trbojevic and Jan Vacek and Alicia Llorente and Felicia Antohe and Viorel Suica and Guillaume Suarez and Ruben T'Kindt and Petra Martin and Deborah Penque and Ines Lanca Martins and Ede Bodoki and Bogdan-Cezar Iacob and Eda Aydindogan and Suna Timur and John Allinson and Christopher Sutton and Theo Luider and Saara Wittfooth and Marei Sammar},

doi = {10.1080/14789450.2020.1763174},

issn = {1744-8387},

year  = {2020},

date = {2020-01-01},

journal = {Expert Review of Proteomics},

pages = {1--17},

abstract = {INTRODUCTION: The importance of biomarkers for pharmaceutical drug development and clinical diagnostics is more significant than ever in the current shift toward personalized medicine. Biomarkers have taken a central position either as companion markers to support drug development and patient selection, or as indicators aiming to detect the earliest perturbations indicative of disease, minimizing therapeutic intervention or even enabling disease reversal. Protein biomarkers are of particular interest given their central role in biochemical pathways. Hence, capabilities to analyze multiple protein biomarkers in one assay are highly interesting for biomedical research. 

AREAS COVERED: We here review multiple methods that are suitable for robust, high throughput, standardized, and affordable analysis of protein biomarkers in a multiplex format. We describe innovative developments in immunoassays, the vanguard of methods in clinical laboratories, and mass spectrometry, increasingly implemented for protein biomarker analysis. Moreover, emerging techniques are discussed with potentially improved protein capture, separation, and detection that will further boost multiplex analyses. 

EXPERT COMMENTARY: The development of clinically applied multiplex protein biomarker assays is essential as multi-protein signatures provide more comprehensive information about biological systems than single biomarkers, leading to improved insights in mechanisms of disease, diagnostics, and the effect of personalized medicine.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{coute_beyond_2020,

title = {Beyond target-decoy competition: stable validation of peptide and protein identifications in mass spectrometry-based discovery proteomics},

author = {Yohann Couté and Christophe Bruley and Thomas Burger},

doi = {10.1021/acs.analchem.0c00328},

issn = {1520-6882},

year  = {2020},

date = {2020-01-01},

journal = {Analytical Chemistry},

abstract = {In bottom-up discovery proteomics, target-decoy competition (TDC) is the most popular method for false discovery rate (FDR) control. Despite unquestionable statistical foundations, this method has drawbacks, including its hitherto unknown intrinsic lack of stability vis-à-vis practical conditions of application. Although some consequences of this instability have already been empirically described, they may have been misinterpreted. This article provides evidence that TDC has become less reliable as the accuracy of modern mass spectrometers improved. We therefore propose to replace TDC by a totally different method to control the FDR at spectrum, peptide and protein levels, while benefiting from the theoretical guarantees of the Benjamini-Hochberg framework. As this method is simpler to use, faster to compute and more stable than TDC, we argue that it is better adapted to the standardization and throughput constraints of current proteomic platforms.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{lacombe_comprehensive_2020,

title = {Comprehensive and comparative exploration of the $backslash$textitAtp7b $^backslashtextrm−/−$ mouse plasma proteome},

author = {Maud Lacombe and Michel Jaquinod and Lucid Belmudes and Yohann Couté and Claire Ramus and Florence Combes and Thomas Burger and Elisabeth Mintz and Justine Barthelon and Vincent Leroy and Aurélia Poujois and Alain Lachaux and France Woimant and Virginie Brun},

url = {http://xlink.rsc.org/?DOI=C9MT00225A},

doi = {10.1039/C9MT00225A},

issn = {1756-5901, 1756-591X},

year  = {2020},

date = {2020-01-01},

journal = {Metallomics},

pages = {10.1039.C9MT00225A},

abstract = {Wilson's disease (WD) is a rare genetic disease caused by mutations in the 

ATP7B 

gene. In this study, we used MS-based proteomics to explore the plasma proteome of the 

Atp7b 

−/− 

mouse, a genetic and phenotypic model for WD. 

 

, 

 

Wilson's disease (WD), a rare genetic disease caused by mutations in the 

ATP7B 

gene, is associated with altered expression and/or function of the copper-transporting ATP7B protein, leading to massive toxic accumulation of copper in the liver and brain. The 

Atp7b 

−/− 

mouse, a genetic and phenotypic model of WD, was developed to provide new insights into the pathogenic mechanisms of WD. Many plasma proteins are secreted by the liver, and impairment of liver function can trigger changes to the plasma proteome. High standard proteomics workflows can identify such changes. Here, we explored the plasma proteome of the 

Atp7b 

−/− 

mouse using a mass spectrometry (MS)-based proteomics workflow combining unbiased discovery analysis followed by targeted quantification. Among the 367 unique plasma proteins identified, 7 proteins were confirmed as differentially abundant between 

Atp7b 

−/− 

mice and wild-type littermates, and were directly linked to WD pathophysiology (regeneration of liver parenchyma, plasma iron depletion, 

etc. 

). We then adapted our targeted proteomics assay to quantify human orthologues of these proteins in plasma from copper-chelator-treated WD patients. The plasma proteome changes observed in the 

Atp7b 

−/− 

mouse were not confirmed in these samples, except for alpha-1 antichymotrypsin, levels of which were decreased in WD patients compared to healthy individuals. Plasma ceruloplasmin was investigated in both the 

Atp7b 

−/− 

mouse model and human patients; it was significantly decreased in the human form of WD only. In conclusion, MS-based proteomics is a method of choice to identify proteome changes in murine models of disrupted metal homeostasis, and allows their validation in human cohorts.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{jeudy_exploration_2020,

title = {Exploration of the propagation of transpovirons within Mimiviridae reveals a unique example of commensalism in the viral world},

author = {Sandra Jeudy and Lionel Bertaux and Jean-Marie Alempic and Audrey Lartigue and Matthieu Legendre and Lucid Belmudes and Sébastien Santini and Nadège Philippe and Laure Beucher and Emanuele G Biondi and Sissel Juul and Daniel J Turner and Yohann Couté and Jean-Michel Claverie and Chantal Abergel},

doi = {10.1038/s41396-019-0565-y},

issn = {1751-7370},

year  = {2020},

date = {2020-01-01},

journal = {The ISME journal},

volume = {14},

number = {3},

pages = {727--739},

abstract = {Acanthamoeba-infecting Mimiviridae are giant viruses with dsDNA genome up to 1.5 Mb. They build viral factories in the host cytoplasm in which the nuclear-like virus-encoded functions take place. They are themselves the target of infections by 20-kb-dsDNA virophages, replicating in the giant virus factories and can also be found associated with 7-kb-DNA episomes, dubbed transpovirons. Here we isolated a virophage (Zamilon vitis) and two transpovirons respectively associated to B- and C-clade mimiviruses. We found that the virophage could transfer each transpoviron provided the host viruses were devoid of a resident transpoviron (permissive effect). If not, only the resident transpoviron originally isolated from the corresponding virus was replicated and propagated within the virophage progeny (dominance effect). Although B- and C-clade viruses devoid of transpoviron could replicate each transpoviron, they did it with a lower efficiency across clades, suggesting an ongoing process of adaptive co-evolution. We analysed the proteomes of host viruses and virophage particles in search of proteins involved in this adaptation process. This study also highlights a unique example of intricate commensalism in the viral world, where the transpoviron uses the virophage to propagate and where the Zamilon virophage and the transpoviron depend on the giant virus to replicate, without affecting its infectious cycle.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{nguyen_fetuin-and_2020,

title = {Fetuin-A and thyroxin binding globulin predict rituximab response in rheumatoid arthritis patients with insufficient response to anti-TNF$alpha$},

author = {Minh Vu Chuong Nguyen and Anaïs Courtier and Annie Adrait and Federica Defendi and Yohann Couté and Athan Baillet and Lisa Guigue and Jacques-Eric Gottenberg and Chantal Dumestre-Pérard and Virginie Brun and Philippe Gaudin},

doi = {10.1007/s10067-020-05030-6},

issn = {1434-9949},

year  = {2020},

date = {2020-01-01},

journal = {Clinical Rheumatology},

abstract = {OBJECTIVES: Rheumatoid arthritis (RA) is a debilitating disease, but patient management and treatment have been revolutionized since the advent of bDMARDs. However, about one third of RA patients do not respond to specific bDMARD treatment without clear identified reasons. Different bDMARDs must be tried until the right drug is found. Here, we sought to identify a predictive protein signature to stratify patient responsiveness to rituximab (RTX) among patients with an insufficient response to a first anti-TNF$alpha$ treatment. 

METHODS: Serum samples were collected at baseline before RTX initiation. A proteomics study comparing responders and nonresponders was conducted to identify and select potential predictive biomarkers whose concentration was measured by quantitative assays. Logistic regression was performed to determine the best biomarker combination to predict good or nonresponse to RTX (EULAR criteria after 6 months' treatment). 

RESULTS: Eleven biomarkers potentially discriminating between responders and nonresponders were selected following discovery proteomics. Quantitative immunoassays and univariate statistical analysis showed that fetuin-A and thyroxine binding globulin (TBG) presented a good capacity to discriminate between patient groups. A logistic regression analysis revealed that the combination of fetuin-A plus TBG could accurately predict a patient's responsiveness to RTX with an AUC of 0.86, sensitivity of 80%, and a specificity of 79%. 

CONCLUSION: In RA patients for whom a first anti-TNF$alpha$ treatment has failed, the serum abundance of fetuin-A and TBG before initiating RTX treatment is an indicator for their response status at 6 months. ClinicalTrials.gov identifier: NCT01000441.Key Points• Proteomic analysis revealed 11 putative predictive biomarkers to discriminate rituximab responder vs. nonresponder RA patients.• Fetuin-A and TBG are significantly differentially expressed at baseline in rituximab responder vs. nonresponder RA patients.• Algorithm combining fetuin-A and TBG accurately predicts response to rituximab in RA patients with insufficient response to TNFi.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}