@article{RN23,

title = {Pharmacologic Normalization of Pancreatic Cancer-Associated Fibroblast Secretome Impairs Prometastatic Cross-Talk With Macrophages},

author = {R. Samain and A. Brunel and T. Douche and M. Fanjul and S. Cassant-Sourdy and J. Rochotte and J. Cros and C. Neuzillet and J. Raffenne and C. Duluc and A. Perraud and J. Nigri and V. Gigoux and I. Bieche and M. Ponzo and G. Carpentier and I. Cascone and R. Tomasini and H. A. Schmid and M. Mathonnet and R. Nicolle and M. P. Bousquet and Y. Martineau and S. Pyronnet and C. Jean and C. Bousquet},

url = {https://www.ncbi.nlm.nih.gov/pubmed/33482394},

doi = {10.1016/j.jcmgh.2021.01.008},

issn = {2352-345X (Electronic) 2352-345X (Linking)},

year  = {2021},

date = {2021-01-01},

urldate = {2021-01-01},

journal = {Cell Mol Gastroenterol Hepatol},

volume = {11},

number = {5},

pages = {1405-1436},

abstract = {BACKGROUND & AIMS: Cancer-associated fibroblasts (CAFs) from pancreatic adenocarcinoma (PDA) present high protein synthesis rates. CAFs express the G-protein-coupled somatostatin receptor sst1. The sst1 agonist SOM230 blocks CAF protumoral features in vitro and in immunocompromised mice. We have explored here the therapeutic potential of SOM230, and underlying mechanisms, in immunocompetent models of murine PDA mimicking the heavy fibrotic and immunosuppressive stroma observed in patient tumors. METHODS: Large-scale mass spectrometry analyses were performed on media conditioned from 9 patient PDA-derived CAF primary cultures. Spontaneous transgenic and experimental (orthotopic co-graft of tumor cells plus CAFs) PDA-bearing mice were longitudinally ultrasound-monitored for tumor and metastatic progression. Histopathology and flow cytometry analyses were performed on primary tumors and metastases. Stromal signatures were functionally validated through bioinformatics using several published, and 1 original, PDA database. RESULTS: Proteomics on the CAF secretome showed that SOM230 controls stromal activities including inflammatory responses. Among the identified secreted proteins, we validated that colony-stimulating factor 1 (CSF-1) (a macrophage growth factor) was reduced by SOM230 in the tumor and plasma of PDA-harboring mice, alongside intratumor stromal normalization (reduced CAF and macrophage activities), and dramatic metastasis reduction. In transgenic mice, these SOM230 benefits alleviate the chemotherapy-induced (gemcitabine) immunosuppressive stroma reshaping. Mechanistically, SOM230 acts in vivo on CAFs through sst1 to disrupt prometastatic CAF production of CSF-1 and cross-talk with macrophages. We found that in patients, stromal CSF-1 was associated with aggressive PDA forms. CONCLUSIONS: We propose SOM230 as an antimetastatic therapy in PDA for its capacity to remodel the fibrotic and immunosuppressive myeloid stroma. This pharmacotherapy should benefit PDA patients treated with chemotherapies.},

note = {Samain, Remi 

Brunel, Alexia 

Douche, Thibault 

Fanjul, Marjorie 

Cassant-Sourdy, Stephanie 

Rochotte, Julia 

Cros, Jerome 

Neuzillet, Cindy 

Raffenne, Jerome 

Duluc, Camille 

Perraud, Aurelie 

Nigri, Jeremy 

Gigoux, Veronique 

Bieche, Ivan 

Ponzo, Matteo 

Carpentier, Gilles 

Cascone, Ilaria 

Tomasini, Richard 

Schmid, Herbert A 

Mathonnet, Muriel 

Nicolle, Remy 

Bousquet, Marie-Pierre 

Martineau, Yvan 

Pyronnet, Stephane 

Jean, Christine 

Bousquet, Corinne 

eng 

Research Support, Non-U.S. Gov't 

2021/01/23 

Cell Mol Gastroenterol Hepatol. 2021;11(5):1405-1436. doi: 10.1016/j.jcmgh.2021.01.008. Epub 2021 Jan 20.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN14,

title = {Colitis Linked to Endoplasmic Reticulum Stress Induces Trypsin Activity Affecting Epithelial Functions},

author = {N. Sola Tapias and A. Denadai-Souza and C. Rolland-Fourcade and M. Quaranta-Nicaise and C. Blanpied and M. Marcellin and A. Edir and C. Rolland and C. Cirillo and G. Dietrich and L. Alric and G. Portier and S. Kirzin and D. Bonnet and E. Mas and O. Burlet-Schiltz and C. Deraison and C. Bonnart and N. Vergnolle and F. Barreau},

url = {https://www.ncbi.nlm.nih.gov/pubmed/33609354},

doi = {10.1093/ecco-jcc/jjab035},

issn = {1876-4479 (Electronic) 1873-9946 (Linking)},

year  = {2021},

date = {2021-01-01},

urldate = {2021-01-01},

journal = {J Crohns Colitis},

volume = {15},

number = {9},

pages = {1528-1541},

abstract = {BACKGROUND AND AIMS: Intestinal epithelial cells [IECs] from inflammatory bowel disease [IBD] patients exhibit an excessive induction of endoplasmic reticulum stress [ER stress] linked to altered intestinal barrier function and inflammation. Colonic tissues and the luminal content of IBD patients are also characterized by increased serine protease activity. The possible link between ER stress and serine protease activity in colitis-associated epithelial dysfunctions is unknown. We aimed to study the association between ER stress and serine protease activity in enterocytes and its impact on intestinal functions. METHODS: The impact of ER stress induced by Thapsigargin on serine protease secretion was studied using either human intestinal cell lines or organoids. Moreover, treating human intestinal cells with protease-activated receptor antagonists allowed us to investigate ER stress-resulting molecular mechanisms that induce proteolytic activity and alter intestinal epithelial cell biology. RESULTS: Colonic biopsies from IBD patients exhibited increased epithelial trypsin-like activity associated with elevated ER stress. Induction of ER stress in human intestinal epithelial cells displayed enhanced apical trypsin-like activity. ER stress-induced increased trypsin activity destabilized intestinal barrier function by increasing permeability and by controlling inflammatory mediators such as C-X-C chemokine ligand 8 [CXCL8]. The deleterious impact of ER stress-associated trypsin activity was specifically dependent on the activation of protease-activated receptors 2 and 4. CONCLUSIONS: Excessive ER stress in IECs caused an increased release of trypsin activity that, in turn, altered intestinal barrier function, promoting the development of inflammatory process.},

note = {Sola Tapias, Nuria 

Denadai-Souza, Alexandre 

Rolland-Fourcade, Claire 

Quaranta-Nicaise, Muriel 

Blanpied, Catherine 

Marcellin, Marlene 

Edir, Anissa 

Rolland, Corinne 

Cirillo, Carla 

Dietrich, Gilles 

Alric, Laurent 

Portier, Guillaume 

Kirzin, Sylvain 

Bonnet, Delphine 

Mas, Emmanuel 

Burlet-Schiltz, Odile 

Deraison, Celine 

Bonnart, Chrystelle 

Vergnolle, Nathalie 

Barreau, Frederick 

eng 

French Ministry of Research and Technology 

ANR JCJC-11JSV1 001 01-IBDase/National Agency for Research 

ERC- 310973 PIPE/ERC_/European Research Council/International 

ANR-11-EQPX-0003/French government 

England 

2021/02/21 

J Crohns Colitis. 2021 Sep 25;15(9):1528-1541. doi: 10.1093/ecco-jcc/jjab035.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN15,

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

author = {Y. Zhai and J. Celis-Gutierrez and G. Voisinne and D. Mori and L. Girard and O. Burlet-Schiltz and A. G. Peredo and R. Roncagalli and B. Malissen},

url = {https://www.ncbi.nlm.nih.gov/pubmed/33139903},

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

issn = {2042-0226 (Electronic) 1672-7681 (Linking)},

year  = {2021},

date = {2021-01-01},

urldate = {2021-01-01},

journal = {Cell Mol Immunol},

volume = {18},

number = {6},

pages = {1581-1583},

note = {Zhai, Yunhao 

Celis-Gutierrez, Javier 

Voisinne, Guillaume 

Mori, Daiki 

Girard, Laura 

Burlet-Schiltz, Odile 

de Peredo, Anne Gonzalez 

Roncagalli, Romain 

Malissen, Bernard 

eng 

787300/EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council) 

SUPERBASILIC/Agence Nationale de la Recherche (French National Research Agency) 

ANR-11-LABEX-0043/Agence Nationale de la Recherche (French National Research Agency) 

ANR-10-IDEX-0001-02 PSL/Agence Nationale de la Recherche (French National Research Agency) 

ANR-10-INBS-08/Agence Nationale de la Recherche (French National Research Agency) 

Letter 

Research Support, Non-U.S. Gov't 

China 

2020/11/04 

Cell Mol Immunol. 2021 Jun;18(6):1581-1583. doi: 10.1038/s41423-020-00575-7. Epub 2020 Nov 2.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{felix_structural_2021,

title = {Structural and functional analysis of the Francisella lysine decarboxylase as a key actor in oxidative stress resistance},

author = {Jan Felix and Claire Siebert and Julia Novion Ducassou and Jérôme Nigou and Pierre Simon Garcia and Angélique Fraudeau and Karine Huard and Caroline Mas and Céline Brochier-Armanet and Yohann Couté and Irina Gutsche and Patricia Renesto},

url = {http://www.nature.com/articles/s41598-020-79611-5},

doi = {10.1038/s41598-020-79611-5},

issn = {2045-2322},

year  = {2021},

date = {2021-01-01},

urldate = {2021-01-01},

journal = {Scientific Reports},

volume = {11},

number = {1},

pages = {972},

abstract = {Abstract 

 

 Francisella tularensis 

 is one of the most virulent pathogenic bacteria causing the acute human respiratory disease tularemia. While the mechanisms underlying 

 F. tularensis 

 pathogenesis are largely unknown, previous studies have shown that a 

 F. novicida 

 transposon mutant with insertions in a gene coding for a putative lysine decarboxylase was attenuated in mouse spleen, suggesting a possible role of its protein product as a virulence factor. Therefore, we set out to structurally and functionally characterize the 

 F. novicida 

 lysine decarboxylase 

 , 

 which we termed LdcF 

 . 

 Here, we investigate the genetic environment of 

 ldcF 

 as well as its evolutionary relationships with other basic AAT-fold amino acid decarboxylase superfamily members, known as key actors in bacterial adaptative stress response and polyamine biosynthesis. We determine the crystal structure of LdcF and compare it with the most thoroughly studied lysine decarboxylase, 

 E. coli 

 LdcI 

 . 

 We analyze the influence of 

 ldcF 

 deletion on bacterial growth under different stress conditions in dedicated growth media, as well as in infected macrophages, and demonstrate its involvement in oxidative stress resistance. Finally, our mass spectrometry-based quantitative proteomic analysis enables identification of 80 proteins with expression levels significantly affected by 

 ldcF 

 deletion, including several DNA repair proteins potentially involved in the diminished capacity of the 

 F. novicida 

 mutant to deal with oxidative stress. Taken together, we uncover an important role of LdcF in 

 F. novicida 

 survival in host cells through participation in oxidative stress response, thereby singling out this previously uncharacterized protein as a potential drug target.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{takata-tsuji_microglia_2021,

title = {Microglia modulate gliotransmission through the regulation of VAMP2 proteins in astrocytes},

author = {Fuyuko Takata-Tsuji and Naura Chounlamountri and Le-Duy Do and Camille Philippot and Julia Novion Ducassou and Yohann Couté and Sarrah Ben Achour and Jérôme Honnorat and Christophe Place and Olivier Pascual},

doi = {10.1002/glia.23884},

issn = {1098-1136},

year  = {2021},

date = {2021-01-01},

urldate = {2021-01-01},

journal = {Glia},

volume = {69},

number = {1},

pages = {61--72},

abstract = {Vesicular release is one of the release mechanisms of various signaling molecules. In neurons, the molecular machinery involved in vesicular release has been designed through evolution to trigger fast and synchronous release of neurotransmitters. Similar machinery with a slower kinetic and a slightly different molecular assembly allows astrocytes to release various transmitters such as adenosine triphosphate (ATP), glutamate, and D-serine. Astrocytes are important modulators of neurotransmission through gliotransmitter release. We recently demonstrated that microglia, another type of glia, release ATP to modulate synaptic transmission using astrocytes as intermediate. We now report that microglia regulate astrocytic gliotransmission through the regulation of SNARE proteins in astrocytes. Indeed, we found that gliotransmission triggered by P2Y1 agonist is impaired in slices from transgenic mice devoid of microglia. Using total internal reflection fluorescence imaging, we found that the vesicular release of gliotransmitter by astrocytes was different in cultures lacking microglia compared to vesicular release in astrocytes cocultured with microglia. Quantification of the kinetic of vesicular release indicates that the overall release appears to be faster in pure astrocyte cultures with more vesicles close to the membrane when compared to astrocytes cocultured with microglia. Finally, biochemical investigation of SNARE protein expression indicates an upregulation of VAMP2 in absence of microglia. Altogether, these results indicate that microglia seems to be involved in the regulation of an astrocytic phenotype compatible with proper gliotransmission. The mechanisms described in this study could be of importance for central nervous system diseases where microglia are activated.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{adrait_liquid_2021,

title = {Liquid Biopsy of Bile based on Targeted Mass Spectrometry for the Diagnosis of Malignant Biliary Strictures},

author = {Annie Adrait and Jean-Marc Dumonceau and Myriam Delhaye and Isabelle Annessi-Ramseyer and Jean-Louis Frossard and Yohann Couté and Annarita Farina},

doi = {10.1111/cts.12890},

issn = {1752-8062},

year  = {2021},

date = {2021-01-01},

urldate = {2021-01-01},

journal = {Clinical and Translational Science},

volume = {14},

number = {1},

pages = {148--152},

abstract = {Bile holds biomarkers of malignant biliary strictures (MBS) but is unsuited for automated analyzers used in routine diagnostic laboratories. Selected reaction monitoring (SRM) is a flexible high-throughput analytical approach based on targeted mass spectrometry (MS) already implemented in clinical settings. We tested the hypothesis that SRM could be used to quantify cancer biomarkers in human bile. An SRM-based assay was developed to simultaneously quantify up to 37 peptides from 13 bile proteins in a developmental cohort of 15 patients (MBS},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{van_lis_phylogenetic_2021,

title = {Phylogenetic and functional diversity of aldehyde-alcohol dehydrogenases in microalgae},

author = {Robert Lis and Yohann Couté and Sabine Brugière and Nicolas J. Tourasse and Benoist Laurent and Wolfgang Nitschke and Olivier Vallon and Ariane Atteia},

url = {http://link.springer.com/10.1007/s11103-020-01105-9},

doi = {10.1007/s11103-020-01105-9},

issn = {0167-4412, 1573-5028},

year  = {2021},

date = {2021-01-01},

urldate = {2021-01-01},

journal = {Plant Molecular Biology},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{trauchessec_innovative_2021,

title = {An innovative standard for LC-MS-based HCP-profiling and accurate quantity assessment: Application to batch consistency in viral vaccine samples},

author = {Mathieu Trauchessec and Anne Marie Hesse and Alexandra Kraut and Yves Berard and Laura Herment and Tanguy Fortin and Christophe Bruley and Myriam Ferro and Catherine Manin},

doi = {10.1002/pmic.202000152},

issn = {1615-9861},

year  = {2021},

date = {2021-01-01},

urldate = {2021-01-01},

journal = {Proteomics},

pages = {e2000152},

abstract = {Biotherapeutics, molecules produced from biological systems, require rigorous purification steps to remove impurities including host cell proteins (HCPs). Regulatory guidelines require manufacturers to monitor process-related impurities along the purification workflow. Mass spectrometry (MS) has recently been considered as a complementary method to the well-established ELISA for HCPs quantification, since it has the advantage of unambiguously identifying individual HCP. In this study, we developed an innovative standard dedicated to MS-based HCP-profiling analysis in order to monitor the consistency of viral vaccine intermediate purification samples. This standard, termed the HCP-PROFILER standard, is composed of a water-soluble bead (READYBEADSTM technology) which, after being added into the sample, releases unlabeled peptides in controlled amounts. The standard meets three desired criteria: (1) it is composed of multiple peptides, at different concentration levels, allowing construction of a calibration curve covering the dynamic range of HCPs present in the target sample, ensuring quantification accuracy; (2) it demonstrates high batch-to-batch reproducibility, ensuring quantification robustness and consistency over time; and (3) it is easy to use and avoids user-induced analytical biases. In this study, we present the use of the HCP-PROFILER standard for vaccine batches comparison and downstream process performance studies. This article is protected by copyright. All rights reserved.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{rayapuram_chromatin_2021,

title = {Chromatin phosphoproteomics unravels a function for AT-hook motif nuclear localized protein AHL13 in PAMP-triggered immunity},

author = {Naganand Rayapuram and Mai Jarad and Hanna M. Alhoraibi and Jean Bigeard and Aala A. Abulfaraj and Ronny Völz and Kiruthiga Gayathri Mariappan and Marilia Almeida-Trapp and Maria Schlöffel and Emmanuelle Lastrucci and Ludovic Bonhomme and Andrea A. Gust and Axel Mithöfer and Stefan T. Arold and Delphine Pflieger and Heribert Hirt},

doi = {10.1073/pnas.2004670118},

issn = {1091-6490},

year  = {2021},

date = {2021-01-01},

urldate = {2021-01-01},

journal = {Proceedings of the National Academy of Sciences of the United States of America},

volume = {118},

number = {3},

abstract = {In many eukaryotic systems during immune responses, mitogen-activated protein kinases (MAPKs) link cytoplasmic signaling to chromatin events by targeting transcription factors, chromatin remodeling complexes, and the RNA polymerase machinery. So far, knowledge on these events is scarce in plants and no attempts have been made to focus on phosphorylation events of chromatin-associated proteins. Here we carried out chromatin phosphoproteomics upon elicitor-induced activation of Arabidopsis The events in WT were compared with those in mpk3, mpk4, and mpk6 mutant plants to decipher specific MAPK targets. Our study highlights distinct signaling networks involving MPK3, MPK4, and MPK6 in chromatin organization and modification, as well as in RNA transcription and processing. Among the chromatin targets, we characterized the AT-hook motif containing nuclear localized (AHL) DNA-binding protein AHL13 as a substrate of immune MAPKs. AHL13 knockout mutant plants are compromised in pathogen-associated molecular pattern (PAMP)-induced reactive oxygen species production, expression of defense genes, and PAMP-triggered immunity. Transcriptome analysis revealed that AHL13 regulates key factors of jasmonic acid biosynthesis and signaling and affects immunity toward Pseudomonas syringae and Botrytis cinerea pathogens. Mutational analysis of the phosphorylation sites of AHL13 demonstrated that phosphorylation regulates AHL13 protein stability and thereby its immune functions.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{gilquin_peps_2021,

title = {PepS: An Innovative Microfluidic Device for Bedside Whole Blood Processing before Plasma Proteomics Analyses},

author = {Benoit Gilquin and Myriam Cubizolles and Remco Den Dulk and Frédéric Revol-Cavalier and Manuel Alessio and Charles-Elie Goujon and Camille Echampard and Gorka Arrizabalaga and Annie Adrait and Mathilde Louwagie and Patricia Laurent and Fabrice P. Navarro and Yohann Couté and Marie-Line Cosnier and Virginie Brun},

doi = {10.1021/acs.analchem.0c02270},

issn = {1520-6882},

year  = {2021},

date = {2021-01-01},

urldate = {2021-01-01},

journal = {Analytical Chemistry},

volume = {93},

number = {2},

pages = {683--690},

abstract = {Immunoassays have been used for decades in clinical laboratories to quantify proteins in serum and plasma samples. However, their limitations make them inappropriate in some cases. Recently, mass spectrometry (MS) based proteomics analysis has emerged as a promising alternative method when seeking to assess panels of protein biomarkers with a view to providing protein profiles to monitor health status. Up to now, however, translation of MS-based proteomics to the clinic has been hampered by its complexity and the substantial time and human resources necessary for sample preparation. Plasma matrix is particularly tricky to process as it contains more than 3000 proteins with concentrations spanning an extreme dynamic range (1010). To address this preanalytical challenge, we designed a microfluidic device (PepS) automating and accelerating blood sample preparation for bottom-up MS-based proteomics analysis. The microfluidic cartridge is operated through a dedicated compact instrument providing fully automated fluid processing and thermal control. In less than 2 h, the PepS device allows bedside plasma separation from whole blood, volume metering, depletion of albumin, protein digestion with trypsin, and stabilization of tryptic peptides on solid-phase extraction sorbent. For this first presentation, the performance of the PepS device was assessed using discovery proteomics and targeted proteomics, detecting a panel of three protein biomarkers routinely assayed in clinical laboratories (alanine aminotransferase 1, C-reactive protein, and myoglobin). This innovative microfluidic device and its associated instrumentation should help to streamline and simplify clinical proteomics studies.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{kerjouan_control_2021,

title = {Control of SRC molecular dynamics encodes distinct cytoskeletal responses by specifying signaling pathway usage},

author = {Adèle Kerjouan and Cyril Boyault and Christiane Oddou and Edwige Hiriart-Bryant and Alexei Grichine and Alexandra Kraut and Mylène Pezet and Martial Balland and Eva Faurobert and Isabelle Bonnet and Yohann Couté and Bertrand Fourcade and Corinne Albiges-Rizo and Olivier Destaing},

doi = {10.1242/jcs.254599},

issn = {1477-9137},

year  = {2021},

date = {2021-01-01},

urldate = {2021-01-01},

journal = {Journal of Cell Science},

volume = {134},

number = {2},

abstract = {Upon activation by different transmembrane receptors, the same signaling protein can induce distinct cellular responses. A way to decipher the mechanisms of such pleiotropic signaling activity is to directly manipulate the decision-making activity that supports the selection between distinct cellular responses. We developed an optogenetic probe (optoSRC) to control SRC signaling, an example of a pleiotropic signaling node, and we demonstrated its ability to generate different acto-adhesive structures (lamellipodia or invadosomes) upon distinct spatio-temporal control of SRC kinase activity. The occurrence of each acto-adhesive structure was simply dictated by the dynamics of optoSRC nanoclusters in adhesive sites, which were dependent on the SH3 and Unique domains of the protein. The different decision-making events regulated by optoSRC dynamics induced distinct downstream signaling pathways, which we characterized using time-resolved proteomic and network analyses. Collectively, by manipulating the molecular mobility of SRC kinase activity, these experiments reveal the pleiotropy-encoding mechanism of SRC signaling.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Mori2021,

title = {The T cell CD6 receptor operates a multitask signalosome with opposite functions in T cell activation.},

author = {Daiki Mori and Claude Grégoire and Guillaume Voisinne and Javier Celis-Gutierrez and Rudy Aussel and Laura Girard and Mylène Camus and Marlène Marcellin and Jérémy Argenty and Odile Burlet-Schiltz and Frédéric Fiore and Anne Peredo and Marie Malissen and Romain Roncagalli and Bernard Malissen},

doi = {10.1084/jem.20201011},

year  = {2021},

date = {2021-01-01},

journal = {The Journal of experimental medicine},

volume = {218},

number = {2},

abstract = {To determine the respective contribution of the LAT transmembrane adaptor and CD5 and CD6 transmembrane receptors to early TCR signal propagation, diversification, and termination, we describe a CRISPR/Cas9-based platform that uses primary mouse T cells and permits establishment of the composition of their LAT, CD5, and CD6 signalosomes in only 4 mo using quantitative mass spectrometry. We confirmed that positive and negative functions can be solely assigned to the LAT and CD5 signalosomes, respectively. In contrast, the TCR-inducible CD6 signalosome comprised both positive (SLP-76, ZAP70, VAV1) and negative (UBASH3A/STS-2) regulators of T cell activation. Moreover, CD6 associated independently of TCR engagement to proteins that support its implication in inflammatory pathologies necessitating T cell transendothelial migration. The multifaceted role of CD6 unveiled here accounts for past difficulties in classifying it as a coinhibitor or costimulator. Congruent with our identification of UBASH3A within the CD6 signalosome and the view that CD6 constitutes a promising target for autoimmune disease treatment, single-nucleotide polymorphisms associated with human autoimmune diseases have been found in the Cd6 and Ubash3a genes.},

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}

}

@article{chabrolles_hepatitis_2020,

title = {Hepatitis B virus Core protein nuclear interactome identifies SRSF10 as a host RNA-binding protein restricting HBV RNA production},

author = {Hélène Chabrolles and Héloïse Auclair and Serena Vegna and Thomas Lahlali and Caroline Pons and Maud Michelet and Yohann Couté and Lucid Belmudes and Gilliane Chadeuf and Yujin Kim and Ariel Di Bernardo and Pascal Jalaguier and François-Loïc Cosset and Floriane Fusil and Michel Rivoire and Lee D Arnold and Uri Lopatin and Christophe Combet and Fabien Zoulim and David Grierson and Benoit Chabot and Julie Lucifora and David Durantel and Anna Salvetti},

doi = {10.1371/journal.ppat.1008593},

issn = {1553-7374},

year  = {2020},

date = {2020-01-01},

journal = {PLoS pathogens},

volume = {16},

number = {11},

pages = {e1008593},

abstract = {Despite the existence of a preventive vaccine, chronic infection with Hepatitis B virus (HBV) affects more than 250 million people and represents a major global cause of hepatocellular carcinoma (HCC) worldwide. Current clinical treatments, in most of cases, do not eliminate viral genome that persists as a DNA episome in the nucleus of hepatocytes and constitutes a stable template for the continuous expression of viral genes. Several studies suggest that, among viral factors, the HBV core protein (HBc), well-known for its structural role in the cytoplasm, could have critical regulatory functions in the nucleus of infected hepatocytes. To elucidate these functions, we performed a proteomic analysis of HBc-interacting host-factors in the nucleus of differentiated HepaRG, a surrogate model of human hepatocytes. The HBc interactome was found to consist primarily of RNA-binding proteins (RBPs), which are involved in various aspects of mRNA metabolism. Among them, we focused our studies on SRSF10, a RBP that was previously shown to regulate alternative splicing (AS) in a phosphorylation-dependent manner and to control stress and DNA damage responses, as well as viral replication. Functional studies combining SRSF10 knockdown and a pharmacological inhibitor of SRSF10 phosphorylation (1C8) showed that SRSF10 behaves as a restriction factor that regulates HBV RNAs levels and that its dephosphorylated form is likely responsible for the anti-viral effect. Surprisingly, neither SRSF10 knock-down nor 1C8 treatment modified the splicing of HBV RNAs but rather modulated the level of nascent HBV RNA. Altogether, our work suggests that in the nucleus of infected cells HBc interacts with multiple RBPs that regulate viral RNA metabolism. Our identification of SRSF10 as a new anti-HBV restriction factor offers new perspectives for the development of new host-targeted antiviral strategies.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{van_lis_hybrid_2020,

title = {Hybrid cluster proteins in a photosynthetic microalga},

author = {Robert Lis and Sabine Brugière and Carole Baffert and Yohann Couté and Wolfgang Nitschke and Ariane Atteia},

doi = {10.1111/febs.15025},

issn = {1742-4658},

year  = {2020},

date = {2020-01-01},

journal = {The FEBS journal},

volume = {287},

number = {4},

pages = {721--735},

abstract = {Hybrid cluster proteins (HCPs) are metalloproteins characterized by the presence of an iron-sulfur-oxygen cluster. These proteins occur in all three domains of life. In eukaryotes, HCPs have so far been found only in a few anaerobic parasites and photosynthetic microalgae. With respect to all species harboring an HCP, the green microalga Chlamydomonas reinhardtii stands out by the presence of four HCP genes. The study of the gene and protein structures as well as the phylogenetic analyses strongly support a model in which the HCP family in the alga has emerged from a single gene of alpha proteobacterial origin and then expanded by several rounds of duplications. The spectra and redox properties of HCP1 and HCP3, produced heterologously in Escherichia coli, were analyzed by electron paramagnetic resonance spectroscopy on redox-titrated samples. Both proteins contain a [4Fe-4S]-cluster as well as a [4Fe-2O-2S]-hybrid cluster with paramagnetic properties related to those of HCPs from Desulfovibrio species. Immunoblotting experiments combined with mass spectrometry-based proteomics showed that both nitrate and darkness contribute to the strong upregulation of the HCP levels in C. reinhardtii growing under oxic conditions. The link to the nitrate metabolism is discussed in the light of recent data on the potential role of HCP in S-nitrosylation in bacteria.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{adrait_liquid_2020,

title = {Liquid Biopsy of Bile based on Targeted Mass Spectrometry for the Diagnosis of Malignant Biliary Strictures},

author = {Annie Adrait and Jean-Marc Dumonceau and Myriam Delhaye and Isabelle Annessi-Ramseyer and Jean-Louis Frossard and Yohann Coute and Annarita Farina},

doi = {10.1111/cts.12890},

issn = {1752-8062},

year  = {2020},

date = {2020-01-01},

journal = {Clinical and Translational Science},

abstract = {Bile holds biomarkers of malignant biliary strictures (MBS) but is unsuited for automated analyzers used in routine diagnostic laboratories. Selected Reaction Monitoring (SRM) is a flexible high-throughput analytical approach based on targeted mass spectrometry (MS) already implemented in clinical settings. We tested the hypothesis that SRM could be used to quantify cancer biomarkers in human bile. An SRM-based assay was developed to simultaneously quantify up to 37 peptides from 13 bile proteins in a developmental cohort of 15 patients (MBS},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{coute_mass_2020,

title = {Mass Spectrometry-Based Characterization of the Virion Proteome, Phosphoproteome, and Associated Kinase Activity of Human Cytomegalovirus},

author = {Yohann Couté and Alexandra Kraut and Christine Zimmermann and Nicole Büscher and Anne-Marie Hesse and Christophe Bruley and Marco De Andrea and Christina Wangen and Friedrich Hahn and Manfred Marschall and Bodo Plachter},

url = {https://www.mdpi.com/2076-2607/8/6/820},

doi = {10.3390/microorganisms8060820},

issn = {2076-2607},

year  = {2020},

date = {2020-01-01},

journal = {Microorganisms},

volume = {8},

number = {6},

pages = {820},

abstract = {The assembly of human cytomegalovirus (HCMV) virions is an orchestrated process that requires, as an essential prerequisite, the complex crosstalk between viral structural proteins. Currently, however, the mechanisms governing the successive steps in the constitution of virion protein complexes remain elusive. Protein phosphorylation is a key regulator determining the sequential changes in the conformation, binding, dynamics, and stability of proteins in the course of multiprotein assembly. In this review, we present a comprehensive map of the HCMV virion proteome, including a refined view on the virion phosphoproteome, based on previous publications supplemented by new results. Thus, a novel dataset of viral and cellular proteins contained in HCMV virions is generated, providing a basis for future analyses of individual phosphorylation steps and sites involved in the orchestrated assembly of HCMV virion-specific multiprotein complexes. Finally, we present the current knowledge on the activity of pUL97, the HCMV-encoded and virion-associated kinase, in phosphorylating viral and host proteins.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{crespo_multi-omic_2020,

title = {Multi-omic analysis of gametogenesis reveals a novel signature at the promoters and distal enhancers of active genes},

author = {Marion Crespo and Annelaure Damont and Melina Blanco and Emmanuelle Lastrucci and Sara El Kennani and Côme Ialy-Radio and Laila El Khattabi and Samuel Terrier and Mathilde Louwagie and Sylvie Kieffer-Jaquinod and Anne-Marie Hesse and Christophe Bruley and Sophie Chantalat and Jérôme Govin and François Fenaille and Christophe Battail and Julie Cocquet and Delphine Pflieger},

url = {https://academic.oup.com/nar/article/48/8/4115/5809165},

doi = {10.1093/nar/gkaa163},

issn = {0305-1048, 1362-4962},

year  = {2020},

date = {2020-01-01},

journal = {Nucleic Acids Research},

volume = {48},

number = {8},

pages = {4115--4138},

abstract = {Abstract 

Epigenetic regulation of gene expression is tightly controlled by the dynamic modification of histones by chemical groups, the diversity of which has largely expanded over the past decade with the discovery of lysine acylations, catalyzed from acyl-coenzymes A. We investigated the dynamics of lysine acetylation and crotonylation on histones H3 and H4 during mouse spermatogenesis. Lysine crotonylation appeared to be of significant abundance compared to acetylation, particularly on Lys27 of histone H3 (H3K27cr) that accumulates in sperm in a cleaved form of H3. We identified the genomic localization of H3K27cr and studied its effects on transcription compared to the classical active mark H3K27ac at promoters and distal enhancers. The presence of both marks was strongly associated with highest gene expression. Assessment of their co-localization with transcription regulators (SLY, SOX30) and chromatin-binding proteins (BRD4, BRDT, BORIS and CTCF) indicated systematic highest binding when both active marks were present and different selective binding when present alone at chromatin. H3K27cr and H3K27ac finally mark the building of some sperm super-enhancers. This integrated analysis of omics data provides an unprecedented level of understanding of gene expression regulation by H3K27cr in comparison to H3K27ac, and reveals both synergistic and specific actions of each histone modification.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{kloehn_multi-omics_2020,

title = {Multi-omics analysis delineates the distinct functions of sub-cellular acetyl-CoA pools in Toxoplasma gondii},

author = {Joachim Kloehn and Rebecca D Oppenheim and Ghizal Siddiqui and Pieter-Jan De Bock and Sunil Kumar Dogga and Yohann Coute and Mohamed-Ali Hakimi and Darren J Creek and Dominique Soldati-Favre},

url = {https://bmcbiol.biomedcentral.com/articles/10.1186/s12915-020-00791-7},

doi = {10.1186/s12915-020-00791-7},

issn = {1741-7007},

year  = {2020},

date = {2020-01-01},

journal = {BMC Biology},

volume = {18},

number = {1},

pages = {67},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{sansa_optomechanical_2020,

title = {Optomechanical mass spectrometry},

author = {Marc Sansa and Martial Defoort and Ariel Brenac and Maxime Hermouet and Louise Banniard and Alexandre Fafin and Marc Gely and Christophe Masselon and Ivan Favero and Guillaume Jourdan and Sébastien Hentz},

doi = {10.1038/s41467-020-17592-9},

issn = {2041-1723},

year  = {2020},

date = {2020-01-01},

journal = {Nature Communications},

volume = {11},

number = {1},

pages = {3781},

abstract = {Nanomechanical mass spectrometry has proven to be well suited for the analysis of high mass species such as viruses. Still, the use of one-dimensional devices such as vibrating beams forces a trade-off between analysis time and mass resolution. Complex readout schemes are also required to simultaneously monitor multiple resonance modes, which degrades resolution. These issues restrict nanomechanical MS to specific species. We demonstrate here single-particle mass spectrometry with nano-optomechanical resonators fabricated with a Very Large Scale Integration process. The unique motion sensitivity of optomechanics allows designs that are impervious to particle position, stiffness or shape, opening the way to the analysis of large aspect ratio biological objects of great significance such as viruses with a tail or fibrils. Compared to top-down beam resonators with electrical read-out and state-of-the-art mass resolution, we show a three-fold improvement in capture area with no resolution degradation, despite the use of a single resonance mode.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Postic2020,

title = {Probing Protein Interaction Networks by Combining MS-Based Proteomics and Structural Data Integration.},

author = {Guillaume Postic and Julien Marcoux and Victor Reys and Jessica Andreani and Yves Vandenbrouck and Marie-Pierre Bousquet and Emmanuelle Mouton-Barbosa and Sarah Cianférani and Odile Burlet-Schiltz and Raphael Guerois and Gilles Labesse and Pierre Tufféry},

year  = {2020},

date = {2020-01-01},

journal = {Journal of proteome research},

volume = {19},

number = {7},

pages = {2807--2820},

address = {United States},

abstract = {Protein-protein interactions play a major role in the molecular machinery of life, and various techniques such as AP-MS are dedicated to their identification. However, those techniques return lists of proteins devoid of organizational structure, not detailing which proteins interact with which others. Proposing a hierarchical view of the interactions between the members of the flat list becomes highly tedious for large data sets when done by hand. To help hierarchize this data, we introduce a new bioinformatics protocol that integrates information of the multimeric protein 3D structures available in the Protein Data Bank using remote homology detection, as well as information related to Short Linear Motifs and interaction data from the BioGRID. We illustrate on two unrelated use-cases of different complexity how our approach can be useful to decipher the network of interactions hidden in the list of input proteins, and how it provides added value compared to state-of-the-art resources such as Interactome3D or STRING. Particularly, we show the added value of using homology detection to distinguish between orthologs and paralogs, and to distinguish between core obligate and more facultative interactions. We also demonstrate the potential of considering interactions occurring through Short Linear Motifs.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{dia_reduced_2020,

title = {Reduced reticulum–mitochondria Ca2+ transfer is an early and reversible trigger of mitochondrial dysfunctions in diabetic cardiomyopathy},

author = {Maya Dia and Ludovic Gomez and Helene Thibault and Nolwenn Tessier and Christelle Leon and Christophe Chouabe and Sylvie Ducreux and Noelle Gallo-Bona and Emily Tubbs and Nadia Bendridi and Stephanie Chanon and Aymeric Leray and Lucid Belmudes and Yohann Couté and Mazen Kurdi and Michel Ovize and Jennifer Rieusset and Melanie Paillard},

url = {http://link.springer.com/10.1007/s00395-020-00835-7},

doi = {10.1007/s00395-020-00835-7},

issn = {0300-8428, 1435-1803},

year  = {2020},

date = {2020-01-01},

journal = {Basic Research in Cardiology},

volume = {115},

number = {6},

pages = {74},

abstract = {Abstract 

 

Type 2 diabetic cardiomyopathy features Ca 

2+ 

signaling abnormalities, notably an altered mitochondrial Ca 

2+ 

handling. We here aimed to study if it might be due to a dysregulation of either the whole Ca 

2+ 

homeostasis, the reticulum–mitochondrial Ca 

2+ 

coupling, and/or the mitochondrial Ca 

2+ 

entry through the uniporter. Following a 16-week high-fat high-sucrose diet (HFHSD), mice developed cardiac insulin resistance, fibrosis, hypertrophy, lipid accumulation, and diastolic dysfunction when compared to standard diet. Ultrastructural and proteomic analyses of cardiac reticulum–mitochondria interface revealed tighter interactions not compatible with Ca 

2+ 

transport in HFHSD cardiomyocytes. Intramyocardial adenoviral injections of Ca 

2+ 

sensors were performed to measure Ca 

2+ 

fluxes in freshly isolated adult cardiomyocytes and to analyze the direct effects of in vivo type 2 diabetes on cardiomyocyte function. HFHSD resulted in a decreased IP3R–VDAC interaction and a reduced IP3-stimulated Ca 

2+ 

transfer to mitochondria, with no changes in reticular Ca 

2+ 

level, cytosolic Ca 

2+ 

transients, and mitochondrial Ca 

2+ 

uniporter function. Disruption of organelle Ca 

2+ 

exchange was associated with decreased mitochondrial bioenergetics and reduced cell contraction, which was rescued by an adenovirus-mediated expression of a reticulum-mitochondria linker. An 8-week diet reversal was able to restore cardiac insulin signaling, Ca 

2+ 

transfer, and cardiac function in HFHSD mice. Therefore, our study demonstrates that the reticulum–mitochondria Ca 

2+ 

miscoupling may play an early and reversible role in the development of diabetic cardiomyopathy by disrupting primarily the mitochondrial bioenergetics. A diet reversal, by counteracting the MAM-induced mitochondrial Ca 

2+ 

dysfunction, might contribute to restore normal cardiac function and prevent the exacerbation of diabetic cardiomyopathy.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{began_rhomboid_2020,

title = {Rhomboid intramembrane protease YqgP licenses bacterial membrane protein quality control as adaptor of FtsH textlessspan style=},

author = {Jakub Began and Baptiste Cordier and Jana Březinová and Jordan Delisle and Rozálie Hexnerová and Pavel Srb and Petra Rampírová and Milan Kožíšek and Mathieu Baudet and Yohann Couté and Anne Galinier and Václav Veverka and Thierry Doan and Kvido Strisovsky},

url = {https://onlinelibrary.wiley.com/doi/abs/10.15252/embj.2019102935},

doi = {10.15252/embj.2019102935},

issn = {0261-4189, 1460-2075},

year  = {2020},

date = {2020-01-01},

journal = {The EMBO Journal},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{lezzerini_ribosomal_2020,

title = {Ribosomal protein gene RPL9 variants can differentially impair ribosome function and cellular metabolism},

author = {Marco Lezzerini and Marianna Penzo and Marie-Françoise O'Donohue and Carolina Marques Dos Santos Vieira and Manon Saby and Hyung L Elfrink and Illja J Diets and Anne-Marie Hesse and Yohann Couté and Marc Gastou and Alexandra Nin-Velez and Peter G J Nikkels and Alexandra N Olson and Evelien Zonneveld-Huijssoon and Marjolijn C J Jongmans and GuangJun Zhang and Michel Weeghel and Riekelt H Houtkooper and Marcin W Wlodarski and Roland P Kuiper and Marc B Bierings and Jutte Werff Ten Bosch and Thierry Leblanc and Lorenzo Montanaro and Jonathan D Dinman and Lydie Da Costa and Pierre-Emmanuel Gleizes and Alyson W MacInnes},

doi = {10.1093/nar/gkz1042},

issn = {1362-4962},

year  = {2020},

date = {2020-01-01},

journal = {Nucleic Acids Research},

volume = {48},

number = {2},

pages = {770--787},

abstract = {Variants in ribosomal protein (RP) genes drive Diamond-Blackfan anemia (DBA), a bone marrow failure syndrome that can also predispose individuals to cancer. Inherited and sporadic RP gene variants are also linked to a variety of phenotypes, including malignancy, in individuals with no anemia. Here we report an individual diagnosed with DBA carrying a variant in the 5'UTR of RPL9 (uL6). Additionally, we report two individuals from a family with multiple cancer incidences carrying a RPL9 missense variant. Analysis of cells from these individuals reveals that despite the variants both driving pre-rRNA processing defects and 80S monosome reduction, the downstream effects are remarkably different. Cells carrying the 5'UTR variant stabilize TP53 and impair the growth and differentiation of erythroid cells. In contrast, ribosomes incorporating the missense variant erroneously read through UAG and UGA stop codons of mRNAs. Metabolic profiles of cells carrying the 5'UTR variant reveal an increased metabolism of amino acids and a switch from glycolysis to gluconeogenesis while those of cells carrying the missense variant reveal a depletion of nucleotide pools. These findings indicate that variants in the same RP gene can drive similar ribosome biogenesis defects yet still have markedly different downstream consequences and clinical impacts.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{crespo_systematic_2020,

title = {Systematic genetic and proteomic screens during gametogenesis identify H2BK34 methylation as an evolutionary conserved meiotic mark},

author = {Marion Crespo and Lacey J Luense and Marie Arlotto and Hu Jialei and Jean Dorsey and Encar Garcia-Oliver and Parisha P Shah and Delphine Pflieger and Shelley L Berger and Jérôme Govin},

url = {https://epigeneticsandchromatin.biomedcentral.com/articles/10.1186/s13072-020-00349-5#citeas},

doi = {10.1186/s13072-020-00349-5},

year  = {2020},

date = {2020-01-01},

journal = {Epigenetics & Chromatin},

volume = {13},

number = {35},

pages = {1--23},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{hahn_target_2020,

title = {Target verification of artesunate-related antiviral drugs: assessing the role of mitochondrial and regulatory proteins by click chemistry and fluorescence labeling},

author = {Friedrich Hahn and Aischa Niesar and Christina Wangen and Markus Wild and Benedikt Grau and Lars Herrmann and Aysun Capci and Annie Adrait and Yohann Couté and Svetlana B Tsogoeva and Manfred Marschall},

url = {https://linkinghub.elsevier.com/retrieve/pii/S0166354220302758},

doi = {10.1016/j.antiviral.2020.104861},

issn = {01663542},

year  = {2020},

date = {2020-01-01},

journal = {Antiviral Research},

pages = {104861},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{vandenbrouck_functionally_2020,

title = {The Functionally Unannotated Proteome of Human Male Tissues: A Shared Resource to Uncover New Protein Functions Associated with Reproductive Biology},

author = {Yves Vandenbrouck and Charles Pineau and Lydie Lane},

doi = {10.1021/acs.jproteome.0c00516},

issn = {1535-3907},

year  = {2020},

date = {2020-01-01},

journal = {Journal of Proteome Research},

abstract = {In the context of the Human Proteome Project, we built an inventory of 412 functionally unannotated human proteins for which experimental evidence at the protein level exists (uPE1) and which are highly expressed in tissues involved in human male reproduction. We implemented a strategy combining literature mining, bioinformatics tools to collate annotation and experimental information from specific molecular public resources, and efficient visualization tools to put these unknown proteins into their biological context (protein complexes, tissue and subcellular location, expression pattern). The gathered knowledge allowed pinpointing five uPE1 for which a function has recently been proposed and which should be updated in protein knowledge bases. Furthermore, this bioinformatics strategy allowed to build new functional hypotheses for five other uPE1s in link with phenotypic traits that are specific to male reproductive function such as ciliogenesis/flagellum formation in germ cells (CCDC112 and TEX9), chromatin remodeling (C3orf62) and spermatozoon maturation (CCDC183). We also discussed the enigmatic case of MAGEB proteins, a poorly documented cancer/testis antigen subtype. Tools used and computational outputs produced during this study are freely accessible via ProteoRE (http://www.proteore.org), a Galaxy-based instance, for reuse purposes. We propose these five uPE1s should be investigated in priority by expert laboratories and hope that this inventory and shared resources will stimulate the interest of the community of reproductive biology.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}