15 results on '"Tricot, Sabine"'
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2. Additional file of Clostridium sticklandii, a specialist in amino acid degradation:revisiting its metabolism through its genome sequence
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Fonknechten, Nuria, Chaussonnerie, Sébastien, Tricot, Sabine, Lajus, Aurélie, Andreesen, Jan R, Perchat, Nadia, Pelletier, Eric, Gouyvenoux, Michel, Barbe, Valérie, Salanoubat, Marcel, Paslier, Denis Le, Weissenbach, Jean, Cohen, Georges N, and Kreimeyer, Annett
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humanities - Abstract
Additional file of Clostridium sticklandii, a specialist in amino acid degradation:revisiting its metabolism through its genome sequence
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- 2021
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3. Additional file 11 of Clostridium sticklandii, a specialist in amino acid degradation:revisiting its metabolism through its genome sequence
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Fonknechten, Nuria, Chaussonnerie, Sébastien, Tricot, Sabine, Lajus, Aurélie, Andreesen, Jan R, Perchat, Nadia, Pelletier, Eric, Gouyvenoux, Michel, Barbe, Valérie, Salanoubat, Marcel, Paslier, Denis Le, Weissenbach, Jean, Cohen, Georges N, and Kreimeyer, Annett
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Data_FILES - Abstract
Authors’ original file for figure 3
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- 2021
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4. Additional file 5 of Clostridium sticklandii, a specialist in amino acid degradation:revisiting its metabolism through its genome sequence
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Fonknechten, Nuria, Chaussonnerie, Sébastien, Tricot, Sabine, Lajus, Aurélie, Andreesen, Jan R, Perchat, Nadia, Pelletier, Eric, Gouyvenoux, Michel, Barbe, Valérie, Salanoubat, Marcel, Paslier, Denis Le, Weissenbach, Jean, Cohen, Georges N, and Kreimeyer, Annett
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Additional file 5: LC-MS analyses of amino acid utilization during growth. For each amino acid, its presence in the medium was checked at different growth phases (colour graphs). The growth kinetic is represented by a yellow graph. Citrulline, ornithine, alanine and aspartate (indicated by a black frame) were not added to the medium. They appeared as intermediates or products of metabolism from other amino acids. Since the utilization of methionine was not discussed in the article, the graph for this amino acid is not shown. (PPT 1 MB)
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- 2021
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5. Additional file 1 of Clostridium sticklandii, a specialist in amino acid degradation:revisiting its metabolism through its genome sequence
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Fonknechten, Nuria, Chaussonnerie, Sébastien, Tricot, Sabine, Lajus, Aurélie, Andreesen, Jan R, Perchat, Nadia, Pelletier, Eric, Gouyvenoux, Michel, Barbe, Valérie, Salanoubat, Marcel, Paslier, Denis Le, Weissenbach, Jean, Cohen, Georges N, and Kreimeyer, Annett
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Additional file 1: Genomic and metabolic features of C. sticklandii compared with other clostridia. All data are extracted from the MaGe annotations except those of Clostridium sporogenes, which are from the NCBI database. C.stick: Clostridium sticklandii DSM 519; C.acet: Clostridium acetobutylicum ATCC 824; C.beij: Clostridium beijerinckii NCIMB 8052; C.botu: Clostridium botulinum A Hall; C.diff: Clostridium difficile 630; C.kluv: Clostridium kluyveri DSM 555; C.novy: Clostridium novyi NT; C.perf: Clostridium perfringens ATCC 13124; C.phyt: Clostridium phytofermentans ISDg; C.teta: Clostridium tetani E88; C.ther: C. thermocellum ATCC 27405; C.spor: C. sporogenes ATCC 1557; A.meta: Alkaliphilus metalliredigens QYMF; A.orem: Alkaliphilus oremlandii OhILAs; M.ther: Moorella thermoacetica ATCC 39073. *2-ketoacid ferredoxin oxidoreductases. (DOC 63 KB)
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- 2021
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6. Additional file 6 of Clostridium sticklandii, a specialist in amino acid degradation:revisiting its metabolism through its genome sequence
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Fonknechten, Nuria, Chaussonnerie, Sébastien, Tricot, Sabine, Lajus, Aurélie, Andreesen, Jan R, Perchat, Nadia, Pelletier, Eric, Gouyvenoux, Michel, Barbe, Valérie, Salanoubat, Marcel, Paslier, Denis Le, Weissenbach, Jean, Cohen, Georges N, and Kreimeyer, Annett
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Additional file 6: Cell growth of C. sticklandii in three types of media with different amino acid composition. Graph 1: medium containing amino acids that are catabolized in the exponential phase (Pro, Asn, Thr, Ser, Arg, Cys); Graph 2: medium containing amino acids that are catabolized in the exponential and stationary phase (Pro, Asn, Thr, Ser, Arg, Cys, Leu, Iso, Met, Gln, His, Lys); Graph 3: the amino acid combination of this medium is equivalent to the second medium, complemented with amino acids apparently not metabolized (Pro, Asn, Thr, Ser, Arg, Cys, Leu, Iso, Met, Gln, His, Lys, Trp, Val, Phe, Glu). Tyrosine was added to each medium. (PPT 62 KB)
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- 2021
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7. Additional file 10 of Clostridium sticklandii, a specialist in amino acid degradation:revisiting its metabolism through its genome sequence
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Fonknechten, Nuria, Chaussonnerie, Sébastien, Tricot, Sabine, Lajus, Aurélie, Andreesen, Jan R, Perchat, Nadia, Pelletier, Eric, Gouyvenoux, Michel, Barbe, Valérie, Salanoubat, Marcel, Paslier, Denis Le, Weissenbach, Jean, Cohen, Georges N, and Kreimeyer, Annett
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Data_FILES - Abstract
Authors’ original file for figure 2
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- 2021
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8. Additional file 9 of Clostridium sticklandii, a specialist in amino acid degradation:revisiting its metabolism through its genome sequence
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Fonknechten, Nuria, Chaussonnerie, Sébastien, Tricot, Sabine, Lajus, Aurélie, Andreesen, Jan R, Perchat, Nadia, Pelletier, Eric, Gouyvenoux, Michel, Barbe, Valérie, Salanoubat, Marcel, Paslier, Denis Le, Weissenbach, Jean, Cohen, Georges N, and Kreimeyer, Annett
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Data_FILES - Abstract
Authors’ original file for figure 1
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- 2021
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9. Additional file 7 of Clostridium sticklandii, a specialist in amino acid degradation:revisiting its metabolism through its genome sequence
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Fonknechten, Nuria, Chaussonnerie, Sébastien, Tricot, Sabine, Lajus, Aurélie, Andreesen, Jan R, Perchat, Nadia, Pelletier, Eric, Gouyvenoux, Michel, Barbe, Valérie, Salanoubat, Marcel, Paslier, Denis Le, Weissenbach, Jean, Cohen, Georges N, and Kreimeyer, Annett
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Additional file 7: Comparison of the D-proline reductase gene cluster from different clostridial species. White arrows indicate hypothetical proteins or those presumed not to be involved in the D-proline reductase reaction. The letter "U" indicates the presence of selenocysteine. In Clostridium botulinum A Hall, a part of the cluster is duplicated. (PPT 60 KB)
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- 2021
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10. Additional file 4 of Clostridium sticklandii, a specialist in amino acid degradation:revisiting its metabolism through its genome sequence
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Fonknechten, Nuria, Chaussonnerie, Sébastien, Tricot, Sabine, Lajus, Aurélie, Andreesen, Jan R, Perchat, Nadia, Pelletier, Eric, Gouyvenoux, Michel, Barbe, Valérie, Salanoubat, Marcel, Paslier, Denis Le, Weissenbach, Jean, Cohen, Georges N, and Kreimeyer, Annett
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Additional file 4: Comparative analysis of amino acid degradation pathways in several clostridial species. Blast searches (criteria: 30% identity over at least 80% of the length of the reference protein) were performed to determine the presence of the key enzymes in the microorganisms. All protein sequences were taken from C. sticklandii with two exceptions: the sequence of methylaspartate mutase was from Clostridium cochlearium, and that of 2-hydroxyglutaryl-CoA dehydratase from Acidaminococcus fermentans. C.stick: Clostridium sticklandii DSM 519; C.acet: Clostridium acetobutylicum ATCC 824; C.beij: Clostridium beijerinckii NCIMB 8052; C.botu: Clostridium botulinum A Hall; C.diff: Clostridium difficile 630; C.kluv: Clostridium kluyveri DSM 555; C.novy: Clostridium novyi NT; C.perf: Clostridium perfringens ATCC 13124; C.phyt: Clostridium phytofermentans ISDg; C.teta: Clostridium tetani E88; C.ther: C. thermocellum ATCC 27405; C.spor: C. sporogenes ATCC 15579; A.meta: Alkaliphilus metalliredigens QYMF; A.orem: Alkaliphilus oremlandii OhILAs; M.ther: Moorella thermoacetica ATCC 39073; C.coch: Clostridium cochlearium; A.ferm: Acidaminococcus fermentans DSM 20731. The genome of Clostridium cochlearium is not yet sequenced. (DOC 486 KB)
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- 2021
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11. Intradermal vaccination prevents anti-MOG autoimmune encephalomyelitis in macaques
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Fovet, Claire-Maëlle, Stimmer, Lev, Contreras, Vanessa, Horellou, Philippe, Hubert, Audrey, Seddiki, Nabila, Chapon, Catherine, Tricot, Sabine, Leroy, Carole, Flament, Julien, Massonneau, Julie, Tchitchek, Nicolas, 't Hart, Bert, Zurawski, Sandra, Klucar, Peter, Hantraye, Philippe, Deiva, Kumaran, Zurawski, Gérard, Oh, Sangkon, Le Grand, Roger, Serguera, Ché, Service MIRCEN (MIRCEN), Université Paris-Saclay-Institut de Biologie François JACOB (JACOB), Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA), Infectious Diseases Models for Innovative Therapies (IDMIT), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay, Immunologie des Maladies Virales et Autoimmunes (IMVA - U1184), Université Paris-Sud - Paris 11 (UP11)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Biomedical Primate Research Centre [Rijswijk] (BPRC), University of Groningen [Groningen], University Medical Center Groningen [Groningen] (UMCG), Baylor Institute for Immunology Research (BIIR), Mayo Clinic [Scottsdale], Mayo Clinic, Institut du Cerveau = Paris Brain Institute (ICM), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS)-Institut de Biologie François JACOB (JACOB), Immunologie - Immunopathologie - Immunothérapie [CHU Pitié Salpêtrière] (I3), CHU Charles Foix [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU), Institut de Biologie François JACOB (JACOB), Physiopathologie et immunothérapies dans l’infection VIH [Créteil] (Inserm U955 Équipe 16), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)-Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Université Paris-Est Créteil Val-de-Marne - Faculté de médecine (UPEC Médecine), Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Vaccine Research Institute [Créteil, France] (VRI), AP-HP Hôpital Bicêtre (Le Kremlin-Bicêtre), Laboratoire Archéomatériaux et Prévision de l'Altération (LAPA - UMR 3685), Nanosciences et Innovation pour les Matériaux, la Biomédecine et l'Energie (ex SIS2M) (NIMBE UMR 3685), Institut Rayonnement Matière de Saclay (IRAMIS), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)-Institut Rayonnement Matière de Saclay (IRAMIS), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS), IRAMAT - Centre Ernest Babelon (IRAMAT-CEB), Institut de Recherches sur les Archéomatériaux (IRAMAT), Université de Technologie de Belfort-Montbeliard (UTBM)-Université d'Orléans (UO)-Université Bordeaux Montaigne (UBM)-Centre National de la Recherche Scientifique (CNRS)-Université de Technologie de Belfort-Montbeliard (UTBM)-Université d'Orléans (UO)-Université Bordeaux Montaigne (UBM)-Centre National de la Recherche Scientifique (CNRS), Laboratoire des Maladies Neurodégénératives - UMR 9199 (LMN), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS)-Institut de Biologie François JACOB (JACOB), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Centre National de la Recherche Scientifique (CNRS), Hôpital Bicêtre, Immunologie des maladies virales, auto-immunes, hématologiques et bactériennes (IMVA-HB), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay, Institut du Cerveau et de la Moëlle Epinière = Brain and Spine Institute (ICM), Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)
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Research paper ,Encephalomyelitis, Autoimmune, Experimental ,Autoantigens ,TGFβ ,immune system diseases ,Animals ,Humans ,Lymphocytes ,Autoantibodies ,Vaccines ,EAE ,Vaccination ,hemic and immune systems ,Dendritic Cells ,Anti-MOG IgG ,Recombinant Proteins ,nervous system diseases ,Treg ,Phenotype ,nervous system ,Cytokines ,Macaca ,[SDV.IMM]Life Sciences [q-bio]/Immunology ,Myelin-Oligodendrocyte Glycoprotein ,[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC] ,[SDV.IMM.VAC]Life Sciences [q-bio]/Immunology/Vaccinology ,Tolerance ,Macaque - Abstract
International audience; BACKGROUND: Autoimmune demyelinating diseases (ADD) are a major cause of neurological disability due to autoreactive cellular and humoral immune responses against brain antigens. A cure for chronic ADD could be obtained by appropriate immunomodulation.METHODS: We implemented a preclinical scheme to foster immune tolerance to myelin oligodendrocyte glycoprotein (MOG), in a cynomolgus-macaque model of experimental autoimmune encephalomyelitis (EAE), in which administration of recombinant human MOG (rhMOG) elicits brain inflammation mediated by MOG-autoreactive CD4+ lymphocytes and anti-MOG IgG. For immunotherapy, we used a recombinant antibody (Ab) directed against the dendritic cell-asialoglycoprotein receptor (DC-ASGPR) fused either to MOG or a control antigen PSA (prostate-specific antigen).FINDINGS: rhMOG and the anti-DC-ASGPR-MOG were respectively detected in CD1a+ DCs or CD163+ cells in the skin of macaques. Intradermal administration of anti-DC-ASGPR-MOG, but not control anti-DC-ASGPR-PSA, was protective against EAE. The treatment prevented the CD4+ T cell activation and proinflammatory cytokine production observed in controls. Moreover, the administration of anti-DC-ASGPR-MOG induced MOG-specific CD4+CD25+FOXP3+CD39+ regulatory lymphocytes and favoured an upsurge in systemic TGFβ and IL-8 upon rhMOG re-administration in vivo.INTERPRETATION: We show that the delivery of an anti-DC-ASGPR-MOG allows antigen-specific adaptive immune modulation to prevent the breach of immune tolerance to MOG. Our findings pave the way for therapeutic vaccines for long-lasting remission to grave encephalomyelitis with identified autoantigens, such as ADD associated with anti-MOG autoantibodies. FUND: Work supported by the French ANR (ANR-11-INBS-0008 and ANR-10-EQPX-02-01), NIH (NIH 1 R01 AI 105066), the Baylor Scott and White Healthcare System funding and Roche Research Collaborative grants.
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- 2019
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12. Evaluating the Efficiency of Isotope Transmission for Improved Panel Design and a Comparison of the Detection Sensitivities of Mass Cytometer Instruments
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Tricot, Sabine, Meyrand, Mickael, Sammicheli, Chiara, Elhmouzi-Younes, Jamila, Corneau, Aurélien, Bertholet, Sylvie, Malissen, Marie, Le Grand, Roger, Nuti, Sandra, Luche, Hervé, Cosma, Antonio, Plateforme Cytométrie Pitié-Salpêtrière (LUMIC-CYPS), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Unité Mixte de Service d'Imagerie et de Cytométrie [CHU Saint-Antoine] (UMS LUMIC), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Immunologie des Maladies Virales et Autoimmunes (IMVA - U1184), Université Paris-Sud - Paris 11 (UP11)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre d'Immunophénomique (CIPHE), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), EU/EFPIA Innovative Medicines Initiative Joint Undertaking [115308], French Government Program: ``Investissement d'avenir' [ANR-10-EQPX-02-01], Unité Mixte de Service d'Imagerie et de Cytométrie [CHU Saint-Antoine] (UMS LUMIC), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), and Université Paris-Sud - Paris 11 (UP11)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)
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standardization ,Key terms: mass cytometry ,flow cytometry ,[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN] ,CyTOF - Abstract
International audience; The recent introduction of mass cytometry, a technique coupling a cell introduction system generating a stream of single cells with mass spectrometry, has greatly increased the number of parameters that can be measured per single cell. As with all new technology there is a need for dissemination of standardization and quality control procedures. Here, we characterize variations in sensitivity observed across the mass range of a mass cytometer, using different lanthanide tags. We observed a five-fold difference in lanthanide detection over the mass range and demonstrated that each instrument has its own sensitivity pattern. Therefore, the selection of lanthanide combinations is a key step in the establishment of a staining panel for mass cytometry-based experiments, particularly for multicenter studies. We propose the sensitivity pattern as the basis for panel design, instrument standardization and future implementation of normalization algorithms.
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- 2015
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13. Microbial urate catabolism: characterization of HpyO, a non-homologous isofunctional isoform of the flavoprotein urate hydroxylase HpxO
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Michiel, Magalie, Perchat, Nadia, Perret, Alain, Tricot, Sabine, Papeil, Aude, Besnard, Marielle, de Berardinis, Véronique, Salanoubat, Marcel, Fischer, Cécile, Protéines : biochimie structurale et fonctionnelle (PBSF), Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC), Génomique métabolique (UMR 8030), Genoscope - Centre national de séquençage [Evry] (GENOSCOPE), Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS)-Université d'Évry-Val-d'Essonne (UEVE), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay, Université Paris-Saclay-Direction de Recherche Fondamentale (CEA) (DRF (CEA)), and Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université d'Évry-Val-d'Essonne (UEVE)-Centre National de la Recherche Scientifique (CNRS)
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[SDV]Life Sciences [q-bio] ,[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN] ,[SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology ,ComputingMilieux_MISCELLANEOUS - Abstract
International audience; In aerobic cells, urate is oxidized to 5-hydroxyisourateby two distinct enzymes: a coenzyme-independenturate oxidase (EC 1.7.3.3) found in eukaryotes andbacteria like Bacillus subtilis and a prokaryotic flavoproteinurate hydroxylase (HpxO) originally found insome Klebsiella species. More cases of analogous ornon-homologous isofunctional enzymes (NISE) forurate catabolism have been hypothesized by inspectingbacterial genomes. Here, we used a functionalcomplementation approach in which a candidate genefor urate oxidation is integrated by homologousrecombination in the Acinetobacter baylyi ADP1genome at the locus of its original hpxO gene. Catabolismof urate was restored in A. baylyi ADP1 expressinga FAD-dependent protein from Xanthomonascampestris, representing a new urate hydroxylasefamily that we called HpyO. This enzyme was kineticallycharacterized and compared with other HpxOenzymes. In contrast to the latter, HpyO is a typicalMichaelian enzyme. This work provides the firstexperimental evidences for the function of HpyO inbacterial urate catabolism and establishes it as a NISEof HpxO.
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- 2012
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14. Elaboration d'un questionnaire destiné aux personnes âgées et sa validation
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Tricot, Sabine, Laboratoire d'étude des interactions des molécules alimentaires, Institut National de la Recherche Agronomique (INRA), and Institut Universitaire Professionnalisé en Ingénierie de la Santé. Université Henri Poincaré (Nancy 1), FRA.
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[SDV]Life Sciences [q-bio] ,SANTE - Abstract
*INRA CR de Nantes. Service de Documentation. BP 71627, 44316 Nantes Cedex 03 Diffusion du document : INRA CR de Nantes. Service de Documentation. BP 71627, 44316 Nantes Cedex 03 Diplôme : Maîtrise
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- 2000
15. MYD88 L265P Mutation in Waldenstrom's Macroglogulinemia
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Poulain, Stephanie, Roumier, Christophe, Decambron, Audrey, Renneville, Aline, Herbaux, Charles, Bertrand, Elisabeth, Tricot, Sabine, Daudignon, Agnes, Galiegue-Zouitina, Sylvie, Theisen, Olivier, Grardel, Nathalie, Soenen, Valerie, Olivier Nibourel, Roche-Lestienne, Catherine, Quesnel, Bruno, Duthilleul, Patrick, Preudhomme, Claude, and Leleu, Xavier
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Immunology ,Cell Biology ,Hematology ,Biochemistry - Abstract
Abstract 1307 Background. Mutation of MYD88 gene has recently been identified in activated B-cell like diffuse B-cell lymphoma, and enhanced JAK STAT and NF-kB signalling pathways. Whole exome sequencing study in Waldenstrom macroglobulinemia (WM) suggested a high frequency of MYD88 L265P mutation in WM. Although the genetic background is not fully deciphered in WM, the role of NF-kB and JAK STAT pathways has been demonstrated in WM; which underlying mechanisms of deregulation remain to be elucidated. We aimed to analyze MYD88 mutation in exon 5 and to characterize the clinical significance of this genetic alteration in 67 WM. Method. 67 patients (42 males, 25 females) diagnosed with WM were included in this study, along with 9 patients with chronic lymphocytic leukemia (CLL), 4 multiple myeloma (MM) and 9 marginal zone lymphoma (MZL) were also studied. Patients were untreated at time of BM collection and gave informed consent prior to research sampling. Clinical features, immunophenotypic markers using flow cytometry (Matutes score panel, CD38, CD138, CD27, CD80), conventional cytogenetic, FISH and SNP array data (n = 46) were analysed. B cells from bone marrow and T cells from blood were isolated respectively using B cell isolation kit and Pan T isolation kit (Myltenyi Biotech). For DNA sequencing of exon 5 of MYD88, the exon 5 of MYD88 gene was amplified from genomic DNA by PCR. The purified PCR products were directly sequenced in both directions using BigDye® Terminator Cycle Sequencing Kit (Applied Biosystems, CA, USA) and analyzed on the Applied Biosystems 3130xl Genetic Analyzer. Data were analyzed with SeqScape software version 2.5 (Applied Biosystems). Results. MYD88 L265P mutation (MYDmut) was observed in 79% of patients, including homozygous mutation in two patients (3%). MYD88 mutation was not identified in T lymphocytes isolated from 4 WM patients that confirmed MYD88 mutation was acquired in the tumoral cells. We haven't observed any other mutation on exon 5. We then sought for other mechanisms of MYD88 gene alteration, such as copy number alteration (CNA) and copy neutral –loss of heterozygosity (CN-LOH) also considered as an acquired UPD (uniparental disomy) at MYD88 locus. We found an UPD at MYD88 locus in solely one patient (2%), and haven't identified any deletion at 3p22. On the contrary, we observed a gain on chromosome 3 at 3p22 locus (including MYD88 gene) in 7/57 (12%) patients. Taking together, we identified alteration of the MYD88 locus in 85% of patients with WM, by either gain-of-function mutation (79%) or CNA (12%). Interestingly, we found gain on chromosome 3 more frequently in the MYDwildgroup than in the MYDmutgroup (p=0.02). Twenty one percent of the patients with WM had no mutation of MYD (MYDwild), and were characterized with a female predominance, a splenomegaly, gain of chromosome 3 and CD27 expression. We did not observed difference in terms of survival according to the MYD88 mutation status. MYD88 mutation was not related to deletion 6q, gain of 4, deletion 11q, deletion 17p, deletion 13q14 in our study. Interestingly, deletion 7q, a frequent cytogenetic aberration in marginal zone lymphoma, was rare in our series (4/57; 7%) and was independent of MYD88 mutation status (2 in the MYDwild and 2 in the MYDmut) (p=ns). No MYD88 L265P mutation was observed in CLL and MM. In MZL, 1/9 patient without M monoclonal component had a MYDL265p mutation. Conclusion. These results confirm a high frequency of MYD88 L265P mutation in WM that may become a useful biomarker for diagnostic in WM and may help better understand the physiopathogeny of WM. Disclosures: No relevant conflicts of interest to declare.
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