Search results for "Oncogene protein"

showing 10 items of 812 documents

E2F1 interacts with BCL-xL and regulates its subcellular localization dynamics to trigger cell death

2018

International audience; E2F1 is the main pro-apoptotic effector of the pRB-regulated tumor suppressor pathway by promoting the transcription of various pro-apoptotic proteins. We report here that E2F1 partly localizes to mitochondria, where it favors mitochondrial outer membrane permeabilization. E2F1 interacts with BCL-xL independently from its BH3 binding interface and induces a stabilization of BCL-xL at mitochondrial membranes. This prevents efficient control of BCL-xL over its binding partners, in particular over BAK resulting in the induction of cell death. We thus identify a new, non-BH3-binding regulator of BCL-xL localization dynamics that influences its anti-apoptotic activity.

0301 basic medicineProgrammed cell deathTranscription Geneticbcl-X ProteinRegulatorBcl-xL[SDV.CAN]Life Sciences [q-bio]/CancerBCL-xL mobilityMitochondrionBiochemistrylaw.invention[ SDV.CAN ] Life Sciences [q-bio]/CancerE2F1 Subject Category Autophagy & Cell Death03 medical and health sciences[SDV.CAN] Life Sciences [q-bio]/CancerlawBCL-2 familyCell Line TumorGeneticsJournal ArticleHumansE2F1Molecular BiologyCell DeathbiologyManchester Cancer Research CentreEffectorChemistryResearchInstitutes_Networks_Beacons/mcrcScientific ReportsapoptosisSubcellular localizationMitochondriaCell biologyProtein Transportbcl-2 Homologous Antagonist-Killer Protein030104 developmental biologyGene Expression RegulationProto-Oncogene Proteins c-bcl-2biology.proteinSuppressorbiological phenomena cell phenomena and immunityExtracellular SpaceE2F1 Transcription FactorProtein Binding
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The C-terminal Domains of Apoptotic BH3-only Proteins Mediate Their Insertion into Distinct Biological Membranes

2016

Changes in the equilibrium of pro- and anti-apoptotic members of the B-cell lymphoma-2 (Bcl-2) protein family in the mitochondrial outer membrane (MOM) induce structural changes that commit cells to apoptosis. Bcl-2 homology-3 (BH3)-only proteins participate in this process by either activating pro-apoptotic effectors or inhibiting anti-apoptotic components and by promoting MOM permeabilization. The association of BH3-only proteins with MOMs is necessary for the activation and amplification of death signals; however, the nature of this association remains controversial, as these proteins lack a canonical transmembrane sequence. Here we used an in vitro expression system to study the inserti…

0301 basic medicineProtein familyCèl·lulesBiologyBiochemistryMitochondrial Proteins03 medical and health sciencesProtein DomainsMembranes (Biologia)Protein-fragment complementation assayMembrane BiologyMicrosomesProto-Oncogene ProteinsHumansMolecular BiologyAdaptor Proteins Signal TransducingGeneticsBcl-2-Like Protein 11030102 biochemistry & molecular biologyCell MembraneBcl-2 familyProteïnes de membranaMembrane ProteinsBiological membraneCell BiologyFusion proteinTransmembrane proteinCell biology030104 developmental biologyMembraneProto-Oncogene Proteins c-bcl-2Membrane proteinB-cell lymphoma 2 (Bcl-2) family BH3-only apoptosis membrane insertion membrane protein mitochondrial apoptosis transmembrane domainApoptosis Regulatory ProteinsHydrophobic and Hydrophilic InteractionsHeLa CellsJournal of Biological Chemistry
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Mcl-1 and Bok transmembrane domains : Unexpected players in the modulation of apoptosis

2020

The Bcl-2 protein family comprises both proand antiapoptotic members that control the permeabilization of the mitochondrial outer membrane, a crucial step in the modulation of apoptosis. Recent research has demonstrated that the carboxyl-terminal transmembrane domain (TMD) of some Bcl-2 protein family mem-bers can modulate apoptosis; however, the transmembrane interactome of the antiapoptotic protein Mcl-1 remains largely unexplored. Here, we demonstrate that the Mcl-1 TMD forms homooligomers in the mitochondrial membrane, competes with full-length Mcl-1 protein with regards to its antiapoptotic function, and induces cell death in a Bok-dependent manner. While the Bok TMD oligomers locate p…

0301 basic medicineProtein familyMitochondrionBCL-X(L)Endoplasmic ReticulumInteractome114 Physical sciences03 medical and health sciencesBok0302 clinical medicineProtein DomainsMITOCHONDRIAhemic and lymphatic diseasesAnimalsHumansBcl-2Inner mitochondrial membraneMultidisciplinaryCell DeathChemistryEndoplasmic reticulumapoptosisMcl-1PATHWAYSLOCALIZATIONBiological SciencesTransmembrane protein3. Good healthCell biologytransmembraneTransmembrane domainstomatognathic diseasesGLYCOPHORIN-A DIMERIZATION030104 developmental biologyHELIX PACKINGProto-Oncogene Proteins c-bcl-2BAX030220 oncology & carcinogenesisMitochondrial MembranesPROSURVIVAL BCL-2 PROTEINSMOTIFSURVIVALMyeloid Cell Leukemia Sequence 1 Protein1182 Biochemistry cell and molecular biologyBacterial outer membraneHeLa Cells
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Lack of NFATc1 SUMOylation prevents autoimmunity and alloreactivity

2020

A novel transgenic mouse, in which the transcription factor NFATc1 bears lysine-to-arginine mutations that prevent modification by SUMO, develops normally and is healthy. However, SUMO-insensitive NFATc1 transmits strong tolerogenic signals, thus preventing autoimmune and alloimmune T cell responses.

0301 basic medicineProtein sumoylationEncephalomyelitis Autoimmune ExperimentalT cellStem Cells & RegenerationImmunologySUMO proteinAutoimmunityBiologyenvironment and public healthT-Lymphocytes RegulatoryArticleMinor Histocompatibility AntigensMice03 medical and health sciences0302 clinical medicineImmune systemNeuroinflammationAldesleukinSTAT5 Transcription FactormedicineAnimalsImmunology and AllergyTranscription factorMice Knockoutintegumentary systemNFATC Transcription FactorsExperimental autoimmune encephalomyelitisSumoylationNFATmedicine.diseaseCell biologyenzymes and coenzymes (carbohydrates)030104 developmental biologymedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2030220 oncology & carcinogenesisCytokinesPositive Regulatory Domain I-Binding Factor 1Journal of Experimental Medicine
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Interleukin-17A Promotes Lung Tumor Progression through Neutrophil Attraction to Tumor Sites and Mediating Resistance to PD-1 Blockade

2017

Abstract Introduction Proinflammatory cytokine interleukin-17A (IL-17A) is overexpressed in a subset of patients with lung cancer. We hypothesized that IL-17A promotes a protumorigenic inflammatory phenotype and inhibits antitumor immune responses. Methods We generated bitransgenic mice expressing a conditional IL-17A allele along with conditional Kras G12D and performed immune phenotyping of mouse lungs, a survival analysis, and treatment studies with antibodies either blocking programmed cell death 1 (PD-1) or IL-6 or depleting neutrophils. To support the preclinical findings, we analyzed human gene expression data sets and immune profiled patient lung tumors. Results Tumors in IL-17:Kras…

0301 basic medicinePulmonary and Respiratory MedicineChemokineLung NeoplasmsNeutrophilsLymphocytemedicine.medical_treatmentProgrammed Cell Death 1 ReceptorGene ExpressionMice TransgenicGranulocytemedicine.disease_causeArticleProinflammatory cytokineProto-Oncogene Proteins p21(ras)Mice03 medical and health sciencesImmune systemAnimalsHumansMedicineLung cancerbiologybusiness.industryInterleukin-17medicine.disease030104 developmental biologymedicine.anatomical_structureCytokineOncologyMutationImmunologyDisease Progressionbiology.proteinKRASbusinessJournal of Thoracic Oncology
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Cabozantinib targets bone microenvironment modulating human osteoclast and osteoblast functions

2016

Cabozantinib, a c-MET and vascular endothelial growth factor receptor 2 inhibitor, demonstrated to prolong progression free survival and improve skeletal disease-related endpoints in castration-resistant prostate cancer and in metastatic renal carcinoma. Our purpose is to investigate the direct effect of cabozantinib on bone microenvironment using a total human model of primary osteoclasts and osteoblasts.Osteoclasts were differentiated from monocytes isolated from healthy donors; osteoblasts were derived from human mesenchymal stem cells obtained from bone fragments of orthopedic surgery patients. Osteoclast activity was evaluated by tartrate resistant acid phosphatase (TRAP) staining and …

0301 basic medicinePyridines -- pharmacologyPyridinesPyridineImmunoenzyme TechniqueOsteoclastsApoptosisRANK Ligand -- genetics -- metabolismImmunoenzyme Techniqueschemistry.chemical_compoundBone Resorption -- drug therapy -- metabolism -- pathology0302 clinical medicineOsteogenesisCathepsin KMedicineAnilidesAnilides -- pharmacologyOsteoprotegerin -- genetics -- metabolismOsteoclasts -- cytology -- drug effects -- physiologyHuman primary cellCells CulturedTartrate-resistant acid phosphataseReceptor Activator of Nuclear Factor-kappa B -- genetics -- metabolismbiologyProto-Oncogene Proteins c-met -- genetics -- metabolismReceptor Activator of Nuclear Factor-kappa BReverse Transcriptase Polymerase Chain ReactionOsteoblastOsteogenesiOsteoblastCell DifferentiationSciences bio-médicales et agricolesProto-Oncogene Proteins c-metOsteoblasts -- cytology -- drug effects -- physiologymedicine.anatomical_structureCell Differentiation -- drug effectsOncologyRANKL030220 oncology & carcinogenesishuman primary cellsOsteoclastosteoprotegerin (OPG)bone microenvironmentHumanResearch Papermusculoskeletal diseasesmedicine.medical_specialtyCabozantinibBlotting WesternOsteogenesis -- drug effects -- physiologyReal-Time Polymerase Chain ReactionBone resorption03 medical and health sciencesOsteoprotegerinOsteoclastcabozantinibInternal medicineHumansRNA MessengerBone ResorptionCell ProliferationOsteoblastsbusiness.industryRANK LigandAnilideOsteoprotegerinApoptosiBone microenvironment; Cabozantinib; Human primary cells; Osteoprotegerin (OPG); Receptor activator of nuclear factor-kb ligand (RANKL); Anilides; Apoptosis; Blotting Western; Bone Resorption; Cell Differentiation; Cell Proliferation; Cells Cultured; Humans; Immunoenzyme Techniques; Osteoblasts; Osteoclasts; Osteogenesis; Osteoprotegerin; Proto-Oncogene Proteins c-met; Pyridines; RANK Ligand; RNA Messenger; Real-Time Polymerase Chain Reaction; Receptor Activator of Nuclear Factor-kappa B; Reverse Transcriptase Polymerase Chain Reaction; Oncology030104 developmental biologyEndocrinologychemistrybiology.proteinbusinessRNA Messenger -- geneticsreceptor activator of nuclear factor-kb ligand (RANKL)
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Cytoplasmic localization of the cell polarity factor scribble supports liver tumor formation and tumor cell invasiveness

2018

The loss of epithelial cell polarity plays an important role in the development and progression of liver cancer. However, the specific molecular mechanisms supporting tumor initiation and progression are poorly understood. In this study, transcriptome data and immunofluorescence stains of tissue samples derived from hepatocellular carcinoma (HCC) patients revealed that overexpression associated with cytoplasmic localization of the baso-lateral cell polarity complex protein Scribble (Scrib) correlated with poor prognosis of HCC patients. In comparison to HCC cells stably expressing wildtype Scrib (ScribWT), mutated Scrib with enforced cytoplasmic enrichment (ScribP305L) induced AKT signaling…

0301 basic medicineSCRIBCytoplasmCarcinoma HepatocellularTumor initiationBiologyMice03 medical and health sciences0302 clinical medicineCell Line TumorCell polarityPhosphoprotein PhosphatasesAnimalsHumansPTENTensinNeoplasm InvasivenessEpithelial–mesenchymal transitionProtein kinase BHepatologyOncogeneTumor Suppressor ProteinsLiver NeoplasmsCell PolarityMembrane ProteinsNuclear ProteinsMolecular biology3. Good healthCell Transformation Neoplastic030104 developmental biologyLiver030220 oncology & carcinogenesisbiology.proteinCancer researchProto-Oncogene Proteins c-aktSignal TransductionHepatology
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TET3 prevents terminal differentiation of adult NSCs by a non-catalytic action at Snrpn.

2019

Ten-eleven-translocation (TET) proteins catalyze DNA hydroxylation, playing an important role in demethylation of DNA in mammals. Remarkably, although hydroxymethylation levels are high in the mouse brain, the potential role of TET proteins in adult neurogenesis is unknown. We show here that a non-catalytic action of TET3 is essentially required for the maintenance of the neural stem cell (NSC) pool in the adult subventricular zone (SVZ) niche by preventing premature differentiation of NSCs into non-neurogenic astrocytes. This occurs through direct binding of TET3 to the paternal transcribed allele of the imprinted gene Small nuclear ribonucleoprotein-associated polypeptide N (Snrpn), contr…

0301 basic medicineScienceCellular differentiationGeneral Physics and AstronomySubventricular zone02 engineering and technologyBiologyDNA-binding proteinArticleGeneral Biochemistry Genetics and Molecular BiologyCatalysissnRNP Core ProteinsDioxygenases03 medical and health sciencesMiceNeural Stem CellsLateral VentriclesProto-Oncogene ProteinsmedicineAnimalsRNA Small Interferinglcsh:SciencePsychological repressionreproductive and urinary physiologyMultidisciplinarySnRNP Core ProteinsQNeurogenesisBrainCell DifferentiationGeneral Chemistry021001 nanoscience & nanotechnologyNeural stem cellnervous system diseasesCell biologyDNA-Binding Proteins030104 developmental biologymedicine.anatomical_structurenervous systemAstrocyteslcsh:Qbiological phenomena cell phenomena and immunity0210 nano-technologyGenomic imprintingSignal Transduction
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MET/HGF Co-Targeting in Pancreatic Cancer: A Tool to Provide Insight into the Tumor/Stroma Crosstalk

2018

The ‘onco-receptor’ MET (Hepatocyte Growth Factor Receptor) is involved in the activation of the invasive growth program that is essential during embryonic development and critical for wound healing and organ regeneration during adult life. When aberrantly activated, MET and its stroma-secreted ligand HGF (Hepatocyte Growth Factor) concur to tumor onset, progression, and metastasis in solid tumors, thus representing a relevant target for cancer precision medicine. In the vast majority of tumors, wild-type MET behaves as a ‘stress-response’ gene, and relies on ligand stimulation to sustain cancer cell ‘scattering’, invasion, and protection form apoptosis. …

0301 basic medicineStromal cellpancreatic cancerReviewHGF; MET; Metastasis; Pancreatic cancer; Target therapy; Tumor microenvironment; Animals; Hepatocyte Growth Factor; Humans; Neoplasm Metastasis; Pancreatic Neoplasms; Proto-Oncogene Proteins c-metCatalysisMetastasisInorganic Chemistrylcsh:Chemistry03 medical and health sciences0302 clinical medicinePancreatic cancermedicineAnimalsHumansmetastasistumor microenvironmentHGFPhysical and Theoretical ChemistryNeoplasm MetastasisMolecular Biologylcsh:QH301-705.5SpectroscopyTumor microenvironmentbusiness.industryHepatocyte Growth Factortarget therapyOrganic ChemistryGeneral MedicineProto-Oncogene Proteins c-metmedicine.diseaseComputer Science ApplicationsPancreatic Neoplasms030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Tumor progressionHepatocyte Growth Factor Receptor030220 oncology & carcinogenesisCancer cellCancer researchMETHepatocyte growth factorbusinessmedicine.drugInternational Journal of Molecular Sciences
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Telomeres and Telomerase During Human Papillomavirus-Induced Carcinogenesis

2018

Human papillomaviruses (HPVs) belong to a small spherical virus family and are transmitted through direct contact, most often through sexual behavior. More than 200 types of HPV are known, a dozen or so of which are classified as high-risk viruses (HR HPV) and may contribute to the development of cervical cancer. HPV is a small virus with a capsid composed of L1 and L2 proteins, which are crucial for entry to the cell. The infection begins at the basal cell layer and progresses to involve cells from higher layers of the cervical epithelium. E6 and E7 viral proteins are involved in the process of carcinogenesis. They interact with suppressors of oncogenesis, including p53 and Rb proteins. Th…

0301 basic medicineTelomeraseOncogene ProteinsCarcinogenesisCellReview ArticleBiologymedicine.disease_causeRetinoblastoma ProteinVirus03 medical and health sciences0302 clinical medicineGeneticsmedicineHumansTelomerase reverse transcriptasePapillomaviridaeTelomeraseTelomere ShorteningPharmacologyPapillomavirus InfectionsDNA replicationGeneral MedicineOncogene Proteins ViralVirus InternalizationCell Transformation ViralTelomere030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisCancer researchDisease ProgressionMolecular MedicineRNAFemaleTumor Suppressor Protein p53CarcinogenesisMolecular Diagnosis & Therapy
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