Search results for "Ubiquitin."

showing 10 items of 191 documents

FANCD2 modulates the mitochondrial stress response to prevent common fragile site instability

2021

Common fragile sites (CFSs) are genomic regions frequently involved in cancer-associated rearrangements. Most CFSs lie within large genes, and their instability involves transcription- and replication-dependent mechanisms. Here, we uncover a role for the mitochondrial stress response pathway in the regulation of CFS stability in human cells. We show that FANCD2, a master regulator of CFS stability, dampens the activation of the mitochondrial stress response and prevents mitochondrial dysfunction. Genetic or pharmacological activation of mitochondrial stress signaling induces CFS gene expression and concomitant relocalization to CFSs of FANCD2. FANCD2 attenuates CFS gene transcription and pr…

0301 basic medicineGenome instabilitymusculoskeletal diseasesTranscription GeneticQH301-705.5RegulatorMedicine (miscellaneous)MitochondrionBiology[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyGeneral Biochemistry Genetics and Molecular BiologyOxidative PhosphorylationArticle03 medical and health sciences0302 clinical medicineTranscription (biology)Stress Physiologicalhemic and lymphatic diseasesGene expressionFANCD2HumansBiology (General)GeneUbiquitinsChromosomal fragile siteChromosome Fragile SitesChromosome FragilityFanconi Anemia Complementation Group D2 ProteinDNA damage and repair[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyHCT116 CellsCell biologyMitochondriaSettore BIO/18 - Genetica030104 developmental biologyGene Expression Regulation030220 oncology & carcinogenesisUnfolded Protein ResponseGeneral Agricultural and Biological SciencesDNA Damage
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The Role of the Multifunctional BAG3 Protein in Cellular Protein Quality Control and in Disease

2017

In neurons, but also in all other cells the complex proteostasis network is monitored and tightly regulated by the cellular protein quality control (PQC) system. Beyond folding of newly synthesized polypeptides and their refolding upon misfolding the PQC also manages the disposal of aberrant proteins either by the ubiquitin-proteasome machinery or by the autophagic-lysosomal system. Aggregated proteins are primarily degraded by a process termed selective macroautophagy (or aggrephagy). One such recently discovered selective macroautophagy pathway is mediated by the multifunctional HSP70 co-chaperone BAG3 (BCL-2-associated athanogene 3). Under acute stress and during cellular aging, BAG3 in …

0301 basic medicineHuntingtinSOD1AggrephagyReviewBAG3lcsh:RC321-57103 medical and health sciencesCellular and Molecular NeuroscienceUbiquitinselective macroautophagymedicineprotein quality controllcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMolecular BiologyproteostasisbiologyBAG3NeurodegenerationAutophagymedicine.diseaseCell biology030104 developmental biologyProteostasisneurodegenerative disordersbiology.proteinNeuroscienceFrontiers in Molecular Neuroscience
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Nuclear Translocation of RELB Is Increased in Diseased Human Liver and Promotes Ductular Reaction and Biliary Fibrosis in Mice.

2019

Background & Aims Cholangiocyte proliferation and ductular reaction contribute to the onset and progression of liver diseases. Little is known about the role of the transcription factor nuclear factor-κB (NF-κB) in this process. We investigated the activities of the RELB proto-oncogene NF-κB subunit in human cholangiocytes and in mouse models of liver disease characterized by a ductular reaction. Methods We obtained liver tissue samples from patients with primary sclerosing cholangitis, primary biliary cholangitis, hepatitis B or C virus infection, autoimmune hepatitis, alcoholic liver disease, or without these diseases (controls) from a tissue bank in Germany. Tissues were analyzed by immu…

0301 basic medicineLiver CirrhosisMaleAlcoholic liver diseaseCholangiocyte proliferationAutoimmune hepatitisProto-Oncogene MasLiver diseaseMice0302 clinical medicineCarbon TetrachlorideCells CulturedRELBLiver DiseasesGastroenterologyMiddle Aged3. Good healthDeubiquitinating Enzyme CYLDCysteine EndopeptidasesProtein TransportLiverGene Knockdown TechniquesCytokines030211 gastroenterology & hepatologyFemaleCell activationAdultLymphotoxin-betaAdolescentCholangitis SclerosingPrimary sclerosing cholangitis03 medical and health sciencesYoung AdultLymphotoxin beta ReceptormedicineAnimalsHumansRNA MessengerParenchymal TissueAgedCell ProliferationCell NucleusHepatologybusiness.industryTranscription Factor RelBEpithelial CellsDicarbethoxydihydrocollidinemedicine.diseaseFibrosis030104 developmental biologyCancer researchLiver functionBile DuctsbusinessGastroenterology
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Genome-wide profiling of non-smoking-related lung cancer cells reveals common RB1 rearrangements associated with histopathologic transformation in EG…

2020

The etiology and the molecular basis of lung adenocarcinomas (LuADs) in nonsmokers are currently unknown. Furthermore, the scarcity of available primary cultures continues to hamper our biological understanding of non-smoking-related lung adenocarcinomas (NSK-LuADs). We established patient-derived cancer cell (PDC) cultures from metastatic NSK-LuADs, including two pairs of matched EGFR-mutant PDCs before and after resistance to tyrosine kinase inhibitors (TKIs), and then performed whole-exome and RNA sequencing to delineate their genomic architecture. For validation, we analyzed independent cohorts of primary LuADs. In addition to known non-smoker-associated alterations (e.g. RET, ALK, EGFR…

0301 basic medicineLung NeoplasmsEGFRUbiquitin-Protein LigasesAdenocarcinoma of Lungmedicine.disease_cause03 medical and health sciences0302 clinical medicineGermline mutationtyrosine kinase inhibitorsmedicineGenetic predispositionHumanswhole-exome sequencingLung cancerGeneProtein Kinase InhibitorsExome sequencingMutationbusiness.industryEGFR RB1 lung adenocarcinoma nonsmokers tyrosine kinase inhibitors whole-exome sequencingHematologyrespiratory systemmedicine.diseaselung adenocarcinomadigestive system diseasesrespiratory tract diseasesErbB ReceptorsRetinoblastoma Binding Proteins030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer cellMutationCancer researchbusinessRB1Tyrosine kinaseMicrotubule-Associated Proteinsnonsmokers
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Identification of Cysteine Ubiquitylation Sites on the Sec23A Protein of the COPII Complex Required for Vesicle Formation from the ER

2017

Background COPII is a multiprotein complex that surrounds carrier vesicles budding from the Endoplasmic Reticulum and allows the recruitment of secretory proteins. The Sec23a protein plays a crucial role in the regulation of the dynamics of COPII formation ensuring the proper function of the secretory pathway. Objective Since few evidences suggest that ubiquitylation could have a role in the COPII regulation, the present study was aimed to establish whether the Sec23a component of the vesicular envelope COPII could be ubiquitylated. Method Sec23a ubiquitylation was revealed by co-immunoprecipitation experiments. Recombinant Sec23a was gel-purified and analyzed by mass spectrometry subjected…

0301 basic medicineMultiprotein complexUbiquitylationbiologyVescicular transportEndoplasmic reticulumVesicleSEC23AArticleSec23aGeneral Biochemistry Genetics and Molecular BiologyCell biology03 medical and health sciences030104 developmental biologySecretory proteinUbiquitinERESbiology.proteinCOPIICOPIISecretory pathwayThe Open Biochemistry Journal
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The Mouse Cytomegalovirus Gene m42 Targets Surface Expression of the Protein Tyrosine Phosphatase CD45 in Infected Macrophages

2016

The receptor-like protein tyrosine phosphatase CD45 is expressed on the surface of cells of hematopoietic origin and has a pivotal role for the function of these cells in the immune response. Here we report that following infection of macrophages with mouse cytomegalovirus (MCMV) the cell surface expression of CD45 is drastically diminished. Screening of a set of MCMV deletion mutants allowed us to identify the viral gene m42 of being responsible for CD45 down-modulation. Moreover, expression of m42 independent of viral infection upon retroviral transduction of the RAW264.7 macrophage cell line led to comparable regulation of CD45 expression. In immunocompetent mice infected with an m42 del…

0301 basic medicineMuromegalovirusGenes ViralvirusesCell MembranesFluorescent Antibody TechniqueNEDD4Protein tyrosine phosphatasePathology and Laboratory MedicineBiochemistryLigasesWhite Blood CellsMice0302 clinical medicineSpectrum Analysis TechniquesUbiquitinAnimal CellsMedicine and Health SciencesBiology (General)Regulation of gene expressionStainingMice Inbred BALB CbiologyChemistryCell StainingAntigens CD45Herpesviridae InfectionsHuman cytomegalovirusFlow Cytometry3. Good healthEnzymesSpectrophotometryMedical MicrobiologyViral PathogensViruses293T cellsCell linesHuman CytomegalovirusCytophotometryCellular TypesCellular Structures and OrganellesPathogensBiological culturesBIOMEDICINA I ZDRAVSTVO. Temeljne medicinske znanosti.Research ArticleGene Expression Regulation ViralHerpesvirusesMCMV ; m42 ; CD45QH301-705.5Immune CellsImmunologyImmunoblottingDown-RegulationResearch and Analysis MethodsMicrobiologyGene product03 medical and health sciencesVirologyGeneticsAnimalsHumansMolecular BiologyMicrobial PathogensBlood CellsMacrophagesHEK 293 cellsBIOMEDICINE AND HEALTHCARE. Basic Medical Sciences.OrganismsBiology and Life SciencesProteinsMembrane ProteinsProtein phosphatase 2Cell BiologyRC581-607Ubiquitin LigasesMolecular biologyViral Replication030104 developmental biologyHEK293 CellsRAW 264.7 CellsViral replicationSpecimen Preparation and Treatmentbiology.proteinEnzymologyLeukocyte Common AntigensParasitologyImmunologic diseases. AllergyDNA viruses030215 immunology
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New Functions of APC/C Ubiquitin Ligase in the Nervous System and Its Role in Alzheimer’s Disease

2017

The E3 ubiquitin ligase Anaphase Promoting Complex/Cyclosome (APC/C) regulates important processes in cells, such as the cell cycle, by targeting a set of substrates for degradation. In the last decade, APC/C has been related to several major functions in the nervous system, including axon guidance, synaptic plasticity, neurogenesis, and neuronal survival. Interestingly, some of the identified APC/C substrates have been related to neurodegenerative diseases. There is an accumulation of some degradation targets of APC/C in Alzheimer’s disease (AD) brains, which suggests a dysregulation of the protein complex in the disorder. Moreover, recently evidence has been provided for an inactivation o…

0301 basic medicineNervous systemNeurogenesisUbiquitin-Protein LigasesReviewubiquitin ligaseNervous SystemCatalysisAnaphase-Promoting Complex-CyclosomeCdh1 ProteinsInorganic Chemistrylcsh:Chemistry03 medical and health sciencesMiceAlzheimer Diseasemedicineoxidative stressAnimalsHumansPhysical and Theoretical ChemistryMolecular Biologylcsh:QH301-705.5SpectroscopyNeuronsNeuronal PlasticitybiologyOrganic ChemistryNeurodegenerationNeurogenesisCell CycleneurodegenerationGeneral MedicineCell cyclemedicine.diseaseComputer Science ApplicationsUbiquitin ligaseCell biology030104 developmental biologymedicine.anatomical_structurelcsh:Biology (General)lcsh:QD1-999ImmunologyKnockout mouseProteolysisbiology.proteinAxon guidanceAnaphase-promoting complexexcitotoxicityInternational Journal of Molecular Sciences
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Regulation of E2F1 Transcription Factor by Ubiquitin Conjugation

2017

IF 3.226; International audience; Ubiquitination is a post-translational modification that defines the cellular fate of intracellular proteins. It can modify their stability, their activity, their subcellular location, and even their interacting pattern. This modification is a reversible event whose implementation is easy and fast. It contributes to the rapid adaptation of the cells to physiological intracellular variations and to intracellular or environmental stresses. E2F1 (E2 promoter binding factor 1) transcription factor is a potent cell cycle regulator. It displays contradictory functions able to regulate both cell proliferation and cell death. Its expression and activity are tightly…

0301 basic medicineProgrammed cell deathReviewubiquitinationCatalysislcsh:ChemistryInorganic Chemistry03 medical and health sciencesUbiquitinAnimalsHumansE2F1Physical and Theoretical Chemistry[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biologylcsh:QH301-705.5Molecular BiologyTranscription factorSpectroscopybiologyCell growthOrganic ChemistryE2F1 Transcription FactorGeneral MedicineCell cycleComputer Science ApplicationsCell biology030104 developmental biologyE2F1lcsh:Biology (General)lcsh:QD1-999biology.proteinDNA damagecell cycleE2F1 Transcription FactorIntracellularInternational Journal of Molecular Sciences
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Aβ Induces Excitotoxicity Mediated by APC/C-Cdh1 Depletion That Can Be Prevented by Glutaminase Inhibition Promoting Neuronal Survival

2016

AbstractThe E3 ubiquitin ligase anaphase-promoting complex/cyclosome (APC/C) is activated by the fizzy-related protein homolog/CDC20-like protein 1 (cdh1) in post-mitotic neurons. Growing evidence suggests that dysregulation of APC/C-Cdh1 is involved in neurodegenerative diseases. Here we show in neurons that oligomers of amyloid beta (Aβ), a peptide related to Alzheimer’s disease, cause proteasome-dependent degradation of cdh1. This leads to a subsequent increase in glutaminase (a degradation target of APC/C-Cdh1), which causes an elevation of glutamate levels and further intraneuronal Ca2+ dysregulation, resulting in neuronal apoptosis. Glutaminase inhibition prevents glutamate excitotoxi…

0301 basic medicineProteasome Endopeptidase ComplexCell SurvivalAmyloid betaBlotting WesternExcitotoxicityHippocampusmedicine.disease_causeHippocampusArticleAnaphase-Promoting Complex-CyclosomeCdh1 ProteinsAnimals Genetically ModifiedMice03 medical and health sciences0302 clinical medicineGlutaminasemedicineAnimalsRats WistarNeuronsAmyloid beta-PeptidesMultidisciplinarybiologyGlutaminaseCyclin-dependent kinase 5Glutamate receptorCyclin-Dependent Kinase 5Molecular biologyRatsUbiquitin ligase030104 developmental biologyApoptosisbiology.protein030217 neurology & neurosurgeryScientific Reports
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Allopurinol partially prevents disuse muscle atrophy in mice and humans

2018

AbstractDisuse muscle wasting will likely affect everyone in his or her lifetime in response to pathologies such as joint immobilization, inactivity or bed rest. There are no good therapies to treat it. We previously found that allopurinol, a drug widely used to treat gout, protects muscle damage after exhaustive exercise and results in functional gains in old individuals. Thus, we decided to test its effect in the prevention of soleus muscle atrophy after two weeks of hindlimb unloading in mice, and lower leg immobilization following ankle sprain in humans (EudraCT: 2011-003541-17). Our results show that allopurinol partially protects against muscle atrophy in both mice and humans. The pro…

0301 basic medicineProteasome Endopeptidase Complexmedicine.medical_specialtyScience[SDV]Life Sciences [q-bio]Allopurinolmedicine.medical_treatmentAllopurinolHindlimbBed restArticleMice03 medical and health sciences0302 clinical medicineAtrophyPhysical Conditioning AnimalInternal medicineAnimalsHumansMedicineAnkle InjuriesMuscle SkeletalWastingSoleus muscleMultidisciplinaryUbiquitinbusiness.industryQRmedicine.diseaseMuscular Disorders AtrophicMuscle atrophy3. Good healthGoutMuscular Atrophy030104 developmental biologyEndocrinologyHindlimb SuspensionMedicinemedicine.symptombusiness030217 neurology & neurosurgerymedicine.drugScientific Reports
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