Search results for "Oncogene"

showing 10 items of 1005 documents

Viral Bcl2s' transmembrane domain interact with host Bcl2 proteins to control cellular apoptosis

2020

© The Author(s) 2020.

0301 basic medicineProgrammed cell deathScienceProtein domainGeneral Physics and AstronomyApoptosisBiologyVirus-host interactionsArticleGeneral Biochemistry Genetics and Molecular BiologyFluorescenceCell Line03 medical and health sciences0302 clinical medicineProtein Domainsimmune system diseaseshemic and lymphatic diseasesmedicineHumansAmino Acid SequenceAuthor CorrectionPeptide sequenceneoplasmsMultidisciplinaryVirus–host interactionsQCell MembraneGeneral ChemistryViral proteinsmedicine.diseaseControl cellLymphomaCell biologyVirusTransmembrane domain030104 developmental biologyProto-Oncogene Proteins c-bcl-2Cell cultureApoptosisDoxorubicin030220 oncology & carcinogenesisbiological phenomena cell phenomena and immunityProtein MultimerizationHydrophobic and Hydrophilic InteractionsProteïnesProtein Binding
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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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SWATH-MS based quantitative proteomics analysis reveals that curcumin alters the metabolic enzyme profile of CML cells by affecting the activity of m…

2018

Background Chronic myelogenous leukemia (CML) is a myeloproliferative disorder caused by expression of the chimeric BCR-ABL tyrosine kinase oncogene, resulting from the t(9;22) chromosomal translocation. Imatinib (gleevec, STI-571) is a selective inhibitor of BCR-ABL activity highly effective in the treatment of CML. However, even though almost all CML patients respond to treatment with imatinib or third generation inhibitors, these drugs are not curative and need to be taken indefinitely or until patients become resistant. Therefore, to get a definitive eradication of leukemic cells, it is necessary to find novel therapeutic combinations, for achieving greater efficacy and fewer side effec…

0301 basic medicineProteomicsCancer ResearchCurcuminCML cellsCellReceptors Cytoplasmic and NuclearKaryopherinsTransfectionlcsh:RC254-282Mass SpectrometrymiR-22/IPO7/HIF-1α axis03 medical and health scienceschemistry.chemical_compound0302 clinical medicinemiR-22/IPO7/HIF-1α axiSettore BIO/13 - Biologia Applicatahemic and lymphatic diseasesCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineHumansCML cells; Curcumin; miR-22/IPO7/HIF-1α axis; SWATH-MS; Oncology; Cancer ResearchOncogeneChemistryResearchCML cellImatinibTransfectionmedicine.diseaseHypoxia-Inducible Factor 1 alpha Subunitlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens3. Good healthMicroRNAs030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCancer researchCurcuminSWATH-MSK562 CellsTyrosine kinaseK562 cellsChronic myelogenous leukemiamedicine.drug
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KRAS mutations testing in non-small cell lung cancer: the role of Liquid biopsy in the basal setting

2020

In advanced stage non-small cell lung cancer (NSCLC) patients, Kirsten Rat Sarcoma Viral Oncogene Homolog (KRAS) testing may soon acquire a predictive significance to select patients for AMG510 treatment. Since tissue samples are not always available, liquid biopsy may represent a viable option for KRAS testing. Here, we review the last three years clinical practice performed on 194 plasma based liquid biopsies by next generation sequencing (NGS) SiRe(®) panel. In particular, 36 (18.6%) KRAS mutated cases were identified, with an overall median allelic frequency of 5.0% (ranging between 0.2% and 46.8%). No concomitant mutations were observed in the other NSCLC clinical relevant genes includ…

0301 basic medicinePulmonary and Respiratory MedicineAMG510Settore MED/06 - Oncologia MedicaViral Oncogenemedicine.disease_cause03 medical and health sciencesBasal (phylogenetics)0302 clinical medicineG12CMedicineEpidermal growth factor receptorLiquid biopsyLung cancerneoplasmsMutationbiologyLiquid biopsybusiness.industryKirsten Rat Sarcoma Viral Oncogene Homolog (KRAS)Review Article on Improving Outcomes in Lung Cancer Through Early Diagnosis and Smoking Cessationmedicine.diseaseBasal setting030104 developmental biologyNext generation sequencing (NGS)030220 oncology & carcinogenesisCancer researchbiology.proteinBiomarker (medicine)KRASLung cancerbusiness
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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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Anti-angiogenic agents in the age of resistance to immune checkpoint inhibitors: Do they have a role in non-oncogene-addicted non-small cell lung can…

2020

The introduction of licensed front-line immunotherapies has heralded a new era for the treatment of non-oncogene-addicted, advanced non-small cell lung cancer (NSCLC). Yet as with all evolutions in clinical management, changes in practice can outpace the availability of the clinical evidence needed to inform subsequent therapeutic decision making. At the time of writing, there is limited available evidence on the optimum therapeutic options after progression on immunotherapy. Further research is needed to define mechanisms of immunotherapy resistance in patients with advanced NSCLC, and to understand the implications for subsequent treatment response. Pending the availability of robust clin…

0301 basic medicinePulmonary and Respiratory MedicineOncologyCancer Researchmedicine.medical_specialtyLung Neoplasmsmedicine.medical_treatmentNintedanibContext (language use)Angiogenesis InhibitorsAnti-angiogenic drugNon-oncogene-addicted non-small cell lung cancer (NSCLC)03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicineCarcinoma Non-Small-Cell LungmedicineTumor MicroenvironmentHumansTumor microenvironment (TME)Lung cancerImmune Checkpoint InhibitorsTumor microenvironmentAnti-angiogenic drug; Immunotherapy resistance; Nintedanib; Non-oncogene-addicted non-small cell lung cancer (NSCLC); Tumor microenvironment (TME); Vascular endothelial growth factor (VEGF)Oncogenebusiness.industryVascular endothelial growth factor (VEGF)ImmunosuppressionImmunotherapymedicine.diseaseImmunotherapy resistance030104 developmental biologyOncologychemistry030220 oncology & carcinogenesisNintedanibNon small cellImmunotherapybusiness
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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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