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5 results on '"MESH: Thiolester Hydrolases"'

1. Palmitoyl protein thioesterase 1 modulates tumor necrosis factor α-induced apoptosis

Author

Thierry Levade, Frédérique Sabourdy, Nicole Therville, Nathalie Andrieu-Abadie, Anu Jalanko, Virginie Garcia, Claudine Tardy, Institut de médecine moléculaire de Rangueil (I2MR), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées- Institut Fédératif de Recherche Bio-médicale Institution (IFR150)-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire de Biochimie [CHU Toulouse], Institut Fédératif de Biologie (IFB), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Pôle Biologie [CHU Toulouse], Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), Department of Molecular Medicine, National Public Health Institute of Helsinki, and Simon, Marie Francoise

Subjects
MESH: Membrane Glycoproteins, MESH: NF-kappa B, Apoptosis, MESH: Flow Cytometry, MESH: Mice, Knockout, TNF-Related Apoptosis-Inducing Ligand, Mice, Protein depalmitoylation, Staurosporine, MESH: Animals, Palmitoyl protein thioesterase, Skin, Mice, Knockout, Mitogen-Activated Protein Kinase 1, MESH: Receptors, Tumor Necrosis Factor, Type I, Membrane Glycoproteins, Mitogen-Activated Protein Kinase 3, NF-kappa B, PPT1, Flow Cytometry, Lysosome, Cell biology, Neuronal ceroid lipofuscinosis, Cell Transformation, Neoplastic, Receptors, Tumor Necrosis Factor, Type I, Tumor necrosis factor alpha, MESH: Thiolester Hydrolases, MESH: Membrane Proteins, MESH: Molecular Chaperones, MESH: Mitogen-Activated Protein Kinase 3, MESH: TNF-Related Apoptosis-Inducing Ligand, Palmitoylation, MESH: Mitogen-Activated Protein Kinase 1, medicine.drug, Cell death, Programmed cell death, Blotting, Western, Biology, MESH: Skin, Neuronal Ceroid-Lipofuscinoses, medicine, Animals, Humans, MESH: Blotting, Western, Protein kinase A, MESH: Mice, Molecular Biology, MESH: Humans, Tumor Necrosis Factor-alpha, MESH: Apoptosis, Lysosome-Associated Membrane Glycoproteins, Membrane Proteins, Cell Biology, Fibroblasts, Molecular biology, MESH: Neuronal Ceroid-Lipofuscinoses, MESH: Cell Transformation, Neoplastic, MESH: Fibroblasts, MESH: Tumor Necrosis Factor-alpha, biology.protein, Thiolester Hydrolases, Molecular Chaperones
Abstract

International audience; Induction of apoptosis by TNF has recently been shown to implicate proteases from lysosomal origin, the cathepsins. Here, we investigated the role in apoptosis of palmitoyl protein thioesterase 1 (PPT1), another lysosomal enzyme that depalmitoylates proteins. We show that transformed fibroblasts derived from patients with the infantile form of neuronal ceroid lipofuscinosis (INCL), a neurodegenerative disease due to deficient activity of PPT1, are partially resistant to TNF-induced cell death (57-75% cell viability vs. 15-30% for control fibroblasts). TNF-initiated proteolytic cleavage of caspase-8, Bid and caspase-3, as well as cytochrome c release was strongly attenuated in INCL fibroblasts as compared to control cells. Noteworthy, activation of p42/p44 mitogen-activated protein kinase and of transcription factor NF-kappaB by TNF, and induction of cell death by staurosporine or chemotherapeutic drugs in INCL cells were unaffected by PPT1 deficiency. Resistance to TNF-induced apoptosis was also observed in embryonic fibroblasts derived from Ppt1/Cln1-deficient mice but not from mice with a targeted deletion of Cln3 or Cln5. Finally, reconstitution of PPT1 activity in mutant cells was accompanied by resensitization to TNF-induced caspase activation and toxicity. These observations emphasize for the first time the role of PPT1 and, likely, protein depalmitoylation in the regulation of TNF-induced apoptosis.

Published
2009
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2. A TFTC/STAGA Module Mediates Histone H2A and H2B Deubiquitination, Coactivates Nuclear Receptors, and Counteracts Heterochromatin Silencing

Author

Didier Devys, Hendrik G. Stunnenberg, Ken-ichi Takeyama, Yue Zhao, Shigeaki Kato, Laszlo Tora, Xavier Le Guezennec, Roland Schüle, Shun Sawatsubashi, Eric Metzger, Jacques Bonnet, Sofia G. Georgieva, Eriko Suzuki, Guillaume Lang, Aleksey N. Krasnov, Saya Ito, Peney, Maité, Laboratory of Nuclear Signaling, The University of Tokyo (UTokyo)-Institute of Molecular and Cellular Biosciences, Institut de génétique et biologie moléculaire et cellulaire (IGBMC), Université Louis Pasteur - Strasbourg I-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Universitäts-Frauenklinik und Zentrum für Klinische Forschung, Klinikum der Universität Freiburg, Department of Molecular Biology [Nijmegen], Radboud University Medical Center [Nijmegen], Institute of Gene Biology, Russian Academy of Sciences [Moscow] (RAS), and Institute of Molecular and Cellular Biosciences-The University of Tokyo (UTokyo)

Subjects
Transcription, Genetic, MESH: Sequence Homology, Amino Acid, RNA polymerase II, MESH: Amino Acid Sequence, Animals, Genetically Modified, MESH: Histone Acetyltransferases, 0302 clinical medicine, Heterochromatin, Protein Interaction Mapping, Drosophila Proteins, MESH: Animals, MESH: Gene Silencing, p300-CBP Transcription Factors, MESH: Endopeptidases, Promoter Regions, Genetic, Conserved Sequence, Histone Acetyltransferases, 0303 health sciences, MESH: Conserved Sequence, biology, General transcription factor, MESH: Transcription Factors, Position-effect variegation, MESH: p300-CBP Transcription Factors, 3. Good health, Chromatin, SAGA complex, MESH: Promoter Regions (Genetics), MESH: Heterochromatin, Drosophila melanogaster, Receptors, Androgen, 030220 oncology & carcinogenesis, MESH: Receptors, Androgen, MESH: Thiolester Hydrolases, RNA Polymerase II, Transcription Factors, General, Ubiquitin Thiolesterase, MESH: Trans-Activators, MESH: Drosophila Proteins, Recombinant Fusion Proteins, Molecular Sequence Data, MESH: Sequence Alignment, MESH: Transcription Factors, General, MESH: Drosophila melanogaster, Cell Line, MESH: Animals, Genetically Modified, 03 medical and health sciences, Histone H2A, Endopeptidases, [SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology, MESH: Recombinant Fusion Proteins, Animals, Humans, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, Amino Acid Sequence, Gene Silencing, Molecular Biology, 030304 developmental biology, MESH: Humans, MESH: Molecular Sequence Data, Sequence Homology, Amino Acid, MESH: Transcription, Genetic, MESH: Protein Interaction Mapping, Ubiquitination, Histone acetyltransferase, Cell Biology, MESH: Multiprotein Complexes, Molecular biology, MESH: RNA Polymerase II, MESH: Cell Line, Multiprotein Complexes, biology.protein, Trans-Activators, MESH: Ubiquitination, Thiolester Hydrolases, Sequence Alignment, Transcription Factors
Abstract

International audience; Transcriptional activators, several different coactivators, and general transcription factors are necessary to access specific loci in the dense chromatin structure to allow precise initiation of RNA polymerase II (Pol II) transcription. Histone acetyltransferase (HAT) complexes were implicated in loosening the chromatin around promoters and thus in gene activation. Here we demonstrate that the 2 MDa GCN5 HAT-containing metazoan TFTC/STAGA complexes contain a histone H2A and H2B deubiquitinase activity. We have identified three additional subunits of TFTC/STAGA (ATXN7L3, USP22, and ENY2) that form the deubiquitination module. Importantly, we found that this module is an enhancer of position effect variegation in Drosophila. Furthermore, we demonstrate that ATXN7L3, USP22, and ENY2 are required as cofactors for the full transcriptional activity by nuclear receptors. Thus, the deubiquitinase activity of the TFTC/STAGA HAT complex is necessary to counteract heterochromatin silencing and acts as a positive cofactor for activation by nuclear receptors in vivo.

Published
2008
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3. Genetic Variants of FOXP2 and KIAA0319/TTRAP/THEM2 Locus Are Associated with Altered Brain Activation in Distinct Language-Related Regions

Author

Thomas Bourgeron, Philippe Pinel, Mark Lathrop, Antonio Moreno, Le Bihan D, Fabien Fauchereau, Diana Zelenika, Stanislas Dehaene, Jean-Baptiste Poline, Alexis Barbot, Chaire Psychologie cognitive expérimentale, Collège de France (CdF (institution)), Neuroimagerie cognitive - Psychologie cognitive expérimentale (UNICOG-U992), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris Saclay (COmUE)-Institut National de la Santé et de la Recherche Médicale (INSERM), Gènes, Synapses et Cognition (CNRS - UMR3571 ), Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), Génétique humaine et fonctions cognitives - Human Genetics and Cognitive Functions (GHFC (UMR_3571 / U-Pasteur_1)), Institut Pasteur [Paris]-Université Paris Diderot - Paris 7 (UPD7)-Centre National de la Recherche Scientifique (CNRS), Université de Tsukuba = University of Tsukuba, Service NEUROSPIN (NEUROSPIN), 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 Génotypage (CNG), Commissariat à l'énergie atomique et aux énergies alternatives (CEA), Modelling brain structure, function and variability based on high-field MRI data (PARIETAL), Inria Saclay - Ile de France, Institut National de Recherche en Informatique et en Automatique (Inria)-Institut National de Recherche en Informatique et en Automatique (Inria)-Service NEUROSPIN (NEUROSPIN), 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)), This work was supported by the Pasteur Institute, the Centre National de Génotypage, Evry, University Denis Diderot Paris 7, INSERM, CEA, CNRS, Collège de France, and Fondation FondaMentale. A.B. was funded by IMAGEN project FP6 and J.-B.P. was partly funded by IMAGEN project FP6. IMAGEN receives research funding from the European Community's Sixth Framework Programme (LSHM-CT-2007-037286), We thank the LBIOM team (L. Hertz-Pannier, V. Joly, S. Roger, K. Ripert, S. Desmidt, and G. Mediouni-Cloarec) and other NeuroSpin investigators for contributing to the fMRI/genetic database by sharing fMRI scanning time and participants with us. We also thank Christophe Lalanne for his advice in statistical analysis., Collège de France - Chaire Psychologie cognitive expérimentale, 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 Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), Institut Pasteur [Paris] (IP)-Université Paris Diderot - Paris 7 (UPD7)-Centre National de la Recherche Scientifique (CNRS), 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), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Inria Saclay - Ile de France, Institut National de Recherche en Informatique et en Automatique (Inria)-Institut National de Recherche en Informatique et en Automatique (Inria), Collège de France (CDF), Collège de France (CdF), Neuroimagerie cognitive (UNICOG-U992), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Sud - Paris 11 (UP11), Gènes, Synapses et Cognition, and University of Tsukuba

Subjects
Male, [SDV]Life Sciences [q-bio], MESH: Frontal Lobe, Functional Laterality, MESH: Magnetic Resonance Imaging, Dyslexia, [SCCO]Cognitive science, 0302 clinical medicine, Image Processing, Computer-Assisted, MESH: Nerve Tissue Proteins, MESH: Genetic Association Studies, Genetics, 0303 health sciences, FOXP2 Gene, General Neuroscience, MESH: Polymorphism, Single Nucleotide, Nuclear Proteins, Forkhead Transcription Factors, FOXP2, Articles, Superior temporal sulcus, MESH: Transcription Factors, Magnetic Resonance Imaging, MESH: Image Processing, Computer-Assisted, Temporal Lobe, Frontal Lobe, DNA-Binding Proteins, MESH: Young Adult, Female, MESH: Thiolester Hydrolases, MESH: Oxygen, Adult, MESH: Dyslexia, Reading disability, Nerve Tissue Proteins, Locus (genetics), Single-nucleotide polymorphism, Biology, MESH: Reading, Polymorphism, Single Nucleotide, Young Adult, 03 medical and health sciences, DCDC2, MESH: Forkhead Transcription Factors, medicine, Humans, MESH: Temporal Lobe, MESH: Functional Laterality, Genetic Association Studies, 030304 developmental biology, MESH: Humans, Phosphoric Diester Hydrolases, MESH: Adult, medicine.disease, MESH: Male, Oxygen, Reading, [SDV.MHEP.PSM]Life Sciences [q-bio]/Human health and pathology/Psychiatrics and mental health, Thiolester Hydrolases, MESH: Female, MESH: Nuclear Proteins, 030217 neurology & neurosurgery, Transcription Factors
Abstract

Recent advances have been made in the genetics of two human communication skills: speaking and reading. Mutations of theFOXP2gene cause a severe form of language impairment and orofacial dyspraxia, while single-nucleotide polymorphisms (SNPs) located within aKIAA0319/TTRAP/THEM2gene cluster and affecting theKIAA0319gene expression are associated with reading disability. Neuroimaging studies of clinical populations point to partially distinct cerebral bases for language and reading impairments. However, alteration ofFOXP2andKIAA0319/TTRAP/THEM2polymorphisms on typically developed language networks has never been explored. Here, we genotyped and scanned 94 healthy subjects using fMRI during a reading task. We studied the correlation of genetic polymorphisms with interindividual variability in brain activation and functional asymmetry in frontal and temporal cortices. InFOXP2, SNPs rs6980093 and rs7799109 were associated with variations of activation in the left frontal cortex. In theKIAA0319/TTRAP/THEM2locus, rs17243157 was associated with asymmetry in functional activation of the superior temporal sulcus (STS). Interestingly, healthy subjects bearing theKIAA0319/TTRAP/THEM2variants previously identified as enhancing the risk of dyslexia showed a reduced left-hemispheric asymmetry of the STS. Our results confirm that bothFOXP2andKIAA0319/TTRAP/THEM2genes play an important role in human language development, but probably through different cerebral pathways. The observed cortical effects mirror previous fMRI results in developmental language and reading disorders, and suggest that a continuum may exist between these pathologies and normal interindividual variability.

Published
2012
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4. Gcn5 and SAGA regulate shelterin protein turnover and telomere maintenance

Author

Didier Devys, Sandy Chang, Boyko S. Atanassov, Yvonne A. Evrard, Sharon Y.R. Dent, Laszlo Tora, Asha S. Multani, Zhijing Zhang, Department of Biochemistry and Molecular Biology, The University of Texas M.D. Anderson Cancer Center [Houston], Program in Genes and Development, Center for Cancer Epigenetics, Department of Genetics, Institut de génétique et biologie moléculaire et cellulaire (IGBMC), Université Louis Pasteur - Strasbourg I-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Department of Hematopathology, and Peney, Maité

Subjects
DNA Repair, MESH: DNA Breaks, Double-Stranded, P300-CBP Transcription Factors, Shelterin Complex, MESH: Telomere-Binding Proteins, Mice, 0302 clinical medicine, DNA Breaks, Double-Stranded, p300-CBP Transcription Factors, MESH: Animals, Telomeric Repeat Binding Protein 1, Cells, Cultured, Telomere-binding protein, Genetics, MESH: DNA Repair, 0303 health sciences, Protein Stability, MESH: Proteasome Endopeptidase Complex, MESH: Telomeric Repeat Binding Protein 1, Telomere, MESH: p300-CBP Transcription Factors, Chromatin, SAGA complex, 030220 oncology & carcinogenesis, MESH: Thiolester Hydrolases, Proteasome Inhibitors, Ubiquitin Thiolesterase, MESH: Cells, Cultured, Telomere-Binding Proteins, Biology, Models, Biological, Article, 03 medical and health sciences, MESH: Protein Stability, Animals, Humans, MESH: Chromosome Aberrations, Transcription factor, Molecular Biology, MESH: Mice, 030304 developmental biology, Chromosome Aberrations, MESH: Humans, MESH: Models, Biological, Cell Biology, Shelterin, enzymes and coenzymes (carbohydrates), MESH: Gene Deletion, Thiolester Hydrolases, MESH: Telomere, Gene Deletion, DNA Damage
Abstract

International audience; Histone acetyltransferases (HATs) play important roles in gene regulation and DNA repair by influencing the accessibility of chromatin to transcription factors and repair proteins. Here, we show that deletion of Gcn5 leads to telomere dysfunction in mouse and human cells. Biochemical studies reveal that depletion of Gcn5 or ubiquitin-specific protease 22 (Usp22), which is another bona fide component of the Gcn5-containing SAGA complex, increases ubiquitination and turnover of TRF1, a primary component of the telomeric shelterin complex. Inhibition of the proteasome or overexpression of USP22 opposes this effect. The USP22 deubiquitinating module requires association with SAGA complexes for activity, and we find that depletion of Gcn5 compromises this association in mammalian cells. Thus, our results indicate that Gcn5 regulates TRF1 levels through effects on Usp22 activity and SAGA integrity.

Published
2009
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5. S18Y polymorphism in the UCH-L1 gene and Parkinson's disease: evidence for an age-dependent relationship

Author

Elbaz, Alexis, Levecque, Clotilde, Clavel, Jacqueline, Vidal, Jean-Sébastien, Richard, Florence, Corrèze, Jean-René, Delemotte, Bernard, Amouyel, Philippe, Alpérovitch, Annick, Chartier-Harlin, Marie-Christine, Tzourio, Christophe, Recherches épidémiologiques en neurologie et psychopathologie, Institut National de la Santé et de la Recherche Médicale (INSERM), Epidémiologie des maladies chroniques: impact des intéractions gène environnement sur la santé des populations, Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille, Droit et Santé-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Recherches épidémiologiques et statistiques sur l'environnement et la santé., Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service de neurologie [Saint-Antoine], Université Pierre et Marie Curie - Paris 6 (UPMC)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU), Mutualité sociale agricole, Secretariat, U754, and Service de neurologie [CHU Saint-Antoine]

Subjects
Adult, Male, MESH: Smoking, Adolescent, Genotype, MESH: Age of Onset, MESH: Environmental Exposure, MESH: Insurance, Health, MESH: Genotype, Risk Factors, MESH: Risk Factors, Surveys and Questionnaires, MESH: Polymorphism, Genetic, Humans, MESH: Pesticides, Age of Onset, Pesticides, Alleles, Aged, MESH: Adolescent, MESH: Age Factors, MESH: Aged, Insurance, Health, Polymorphism, Genetic, MESH: Humans, MESH: Middle Aged, MESH: Questionnaires, MESH: Alleles, Smoking, Age Factors, Parkinson Disease, MESH: Adult, Environmental Exposure, Middle Aged, MESH: Ubiquitin Thiolesterase, MESH: Case-Control Studies, MESH: Male, [SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologie, Case-Control Studies, Female, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, Thiolester Hydrolases, MESH: Thiolester Hydrolases, Ubiquitin Thiolesterase, MESH: Female, MESH: Parkinson Disease
Abstract

International audience; We studied the relationship between Parkinson's disease (PD) and the S18Y polymorphism in the UCH-L1 gene and the effect on this relationship of age at onset, smoking, and pesticides. Patients requested free health coverage for PD to the Mutualit?ociale Agricole (MSA), the French health insurance organization for people whose work is related to agriculture. Controls requested reimbursement of health expenses to the MSA. A maximum of three controls were matched to each case. Analyses included participants with both parents born in Europe. There were no differences in S18Y genotypes between patients (n = 209; 67% SS, 32% SY, 1% YY) and controls (n = 488; 66% SS, 30% SY, 4% YY). The relationship between PD and S18Y was modified by age at onset (P = 0.03). The Y allele was inversely associated with PD for patients with onset before 61 years (odds ratio [OR] = 0.53; 95% confidence interval [CI], 0.29-0.99); there was no association for older patients (62-68 years: OR = 1.21; 95% CI, 0.67-2.20; >68 years: OR = 1.24; 95% CI, 0.67-2.31). Among patients, Y carriers had a later onset than noncarriers (P = 0.04). These findings were not modified or confounded by smoking and pesticides. In this community-based case-control study, carriers of the Y allele were at decreased risk of developing PD at a young age, independently of pesticides and smoking.

Published
2003
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