Search results for "Oncogene"

showing 10 items of 1005 documents

STRIPAK Members Orchestrate Hippo and Insulin Receptor Signaling to Promote Neural Stem Cell Reactivation

2019

Summary Adult stem cells reactivate from quiescence to maintain tissue homeostasis and in response to injury. How the underlying regulatory signals are integrated is largely unknown. Drosophila neural stem cells (NSCs) also leave quiescence to generate adult neurons and glia, a process that is dependent on Hippo signaling inhibition and activation of the insulin-like receptor (InR)/PI3K/Akt cascade. We performed a transcriptome analysis of individual quiescent and reactivating NSCs harvested directly from Drosophila brains and identified the conserved STRIPAK complex members mob4, cka, and PP2A (microtubule star, mts). We show that PP2A/Mts phosphatase, with its regulatory subunit Widerbors…

0301 basic medicinereactivationendocrine systemMitosisNerve Tissue ProteinsProtein Serine-Threonine KinasesBiologyArticleGeneral Biochemistry Genetics and Molecular BiologyAnimals Genetically ModifiedPhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineNeural Stem CellsAnimalsDrosophila ProteinsquiescenceProtein Phosphatase 2lcsh:QH301-705.5Protein kinase BCells CulturedPI3K/AKT/mTOR pathwayTissue homeostasisAdaptor Proteins Signal TransducingCell ProliferationHippo signaling pathwayGene Expression ProfilingHippo signalingInR/PI3K/Akt signalingfungiIntracellular Signaling Peptides and ProteinsBrainSTRIPAK membersProtein phosphatase 2Receptor InsulinNeural stem cellCell biologyDrosophila melanogaster030104 developmental biologylcsh:Biology (General)nervous systemHippo signalingSingle-Cell AnalysisTranscriptomeProto-Oncogene Proteins c-akt030217 neurology & neurosurgeryAdult stem cellCell Reports
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Antiviral Properties of Chemical Inhibitors of Cellular Anti-Apoptotic Bcl-2 Proteins

2017

Viral diseases remain serious threats to public health because of the shortage of effective means of control. To combat the surge of viral diseases, new treatments are urgently needed. Here we show that small-molecules, which inhibit cellular anti-apoptotic Bcl-2 proteins (Bcl-2i), induced the premature death of cells infected with different RNA or DNA viruses, whereas, at the same concentrations, no toxicity was observed in mock-infected cells. Moreover, these compounds limited viral replication and spread. Surprisingly, Bcl-2i also induced the premature apoptosis of cells transfected with viral RNA or plasmid DNA but not of mock-transfected cells. These results suggest that Bcl-2i sensiti…

0301 basic medicinevirusesFAMILY INHIBITORSlcsh:QR1-502Virus Replicationlcsh:Microbiologychemistry.chemical_compoundTranscription (biology)SALIPHENYLHALAMIDEhost responseTRANSCRIPTIONprogrammed cell deathinnate immunity1183 Plant biology microbiology virologySulfonamidesAniline CompoundsapoptosisTransfection3. Good healthInfectious DiseasesProto-Oncogene Proteins c-bcl-2X-L INHIBITORVirus DiseasesvirustauditVirusesRNA ViralBiologyTransfectionta3111Antiviral AgentsArticleCell LineMicrobiology in the medical areaantiviral agent03 medical and health sciencesohjelmoitunut solukuolemaVirologyMikrobiologi inom det medicinska områdetHumansMetabolomicsBenzothiazolesInnate immune systemapoptosis; antiviral agent; innate immunity; host responseZIKA VIRUS-INFECTIONCHRONIC LYMPHOCYTIC-LEUKEMIAPOTENTta1183INFLUENZA-Ata1182RNAIsoquinolinesVirology030104 developmental biologyViral replicationchemistryCell cultureApoptosisCELLSREPLICATIONDNA Viral3111 BiomedicineDNA
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A subset of flavaglines inhibits KRAS nanoclustering and activation.

2020

The RAS oncogenes are frequently mutated in human cancers and among the three isoforms (KRAS, HRAS and NRAS), KRAS is the most frequently mutated oncogene. Here, we demonstrate that a subset of flavaglines, a class of natural anti-tumour drugs and chemical ligands of prohibitins, inhibit RAS GTP loading and oncogene activation in cells at nanomolar concentrations. Treatment with rocaglamide, the first discovered flavagline, inhibited the nanoclustering of KRAS, but not HRAS and NRAS, at specific phospholipid-enriched plasma membrane domains. We further demonstrate that plasma membrane-associated prohibitins directly interact with KRAS, phosphatidylserine and phosphatidic acid, and these int…

:Bioengineering [Engineering]Neuroblastoma RAS viral oncogene homologGene isoformLung NeoplasmsGTP'[SDV]Life Sciences [q-bio]AucunBiology: Biochemistry biophysics & molecular biology [F05] [Life sciences]medicine.disease_causeProto-Oncogene Proteins p21(ras)03 medical and health scienceschemistry.chemical_compound0302 clinical medicineRocaglamideCarcinoma Non-Small-Cell LungmedicineKRASHumansdrug therapy;geneticsgeneticsHRASProhibitin: Biochimie biophysique & biologie moléculaire [F05] [Sciences du vivant]neoplasmsComputingMilieux_MISCELLANEOUS030304 developmental biology0303 health sciencesOncogeneLipid nanoclusterOncogenesCell Biologydigestive system diseases3. Good healthrespiratory tract diseasesPhospholipidchemistry030220 oncology & carcinogenesisMutationCancer researchKRASFlavaglineRocaglamideProhibitinSignal Transduction
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Abstract C75: Overcoming KRAS/LKB1 mutant NSCLC resistance to BET bromodomain inhibitors with gemcitabine or Mcl-1 inhibition

2015

Abstract The purpose of our study was to define a method and mechanism for overcoming the resistance of clinically relevant KRAS-mutant/LKB1-deficient NSCLC cells to the BET-bromodomain inhibitor JQ1. LKB1 (Serine/threonine kinase 11) is mutated with loss of function in conjunction with mutated KRAS in 7-10% of NSCLC. Importantly, KRAS-mutant/LKB1-deficiency is associated with tumor aggressiveness and poor survival in human patients as well as in genetically engineered mouse models. Indeed, although the BET bromodomain inhibitor JQ1 dramatically reduces tumor volume in KRAS mutant mice, it has little effect in KRAS-mutant/LKB1-deficient mice. BET bromodomain proteins are chromatin readers t…

A549 cellCancer ResearchGene knockdownKinaseBiologymedicine.disease_causeGemcitabineBromodomainOncologyApoptosisImmunologymedicineCancer researchOncogene MYCKRASneoplasmsmedicine.drugMolecular Cancer Therapeutics
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Angiotensin II dependent cardiac remodeling in the eel Anguilla anguilla involves the NOS/NO system

2017

Angiotensin II (AngII), the principal effector of the Renin-Angiotensin System (RAS), plays an important role in controlling mammalian cardiac morpho-functional remodelling. In the eel Anguilla anguilla, one month administration of AngII improves cardiac performance and influences the expression and localization of molecules which regulate cell growth. To deeper investigate the morpho-functional chronic influences of AngII on the eel heart and the molecular mechanisms involved, freshwater eels (A. anguilla) were intraperitoneally injected for 2 months with AngII (1 nmol g BW-1). Then the isolated hearts were subjected to morphological and western blotting analyses, and nitrite measurements.…

AT(2) receptor; ERK(1-2); Hsp90; Myocardial growth; NOSTRIN0301 basic medicineMAPK/ERK pathwayCancer ResearchPhysiologyClinical Biochemistry030204 cardiovascular system & hematologyBiochemistrychemistry.chemical_compound0302 clinical medicineEnosMyocardial growthReceptorMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Receptors AngiotensinVentricular RemodelingAngiotensin IIHeartNitric oxide synthaseERKmedicine.anatomical_structurecardiovascular systemCollagenmedicine.medical_specialtyEndotheliumHeart VentriclesHsp90BiologyNitric OxideNitric oxide03 medical and health sciencesInternal medicinemedicineAnimalsHSP90 Heat-Shock ProteinsVentricular remodelingAT receptorNitritesERK(1-2)Anguillamedicine.diseasebiology.organism_classificationNOSTRINAngiotensin II030104 developmental biologyEndocrinologychemistryAT(2) receptorbiology.proteinNitric Oxide SynthaseProto-Oncogene Proteins c-akt
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Isoquercitrin and polyphosphate co-enhance mineralization of human osteoblast-like SaOS-2 cells via separate activation of two RUNX2 cofactors AFT6 a…

2014

Isoquercitrin, a dietary phytoestrogen, is a potential stimulator of bone mineralization used for prophylaxis of osteoporotic disorders. Here we studied the combined effects of isoquercitrin, a cell membrane permeable 3-O-glucoside of quercetin, and polyphosphate [polyP], a naturally occurring inorganic polymer inducing bone formation, on mineralization of human osteoblast-like SaOS-2 cells. Both compounds isoquercitrin and polyP induce at non-toxic concentrations the mineralization process of SaOS-2 cells. Co-incubation experiments revealed that isoquercitrin (at 0.1 and 0.3μM), if given simultaneously with polyP (as Ca(2+) salt; at 3, 10, 30 and 100μM) amplifies the mineralization-enhanci…

Activating transcription factorBiochemistryProto-Oncogene Protein c-ets-103 medical and health sciences0302 clinical medicineCalcification PhysiologicPolyphosphatesCell Line TumormedicineHumansSaos-2 cells030304 developmental biologyPharmacology0303 health sciencesOsteoblastsbiologyATF6OsteoblastDrug SynergismActivating Transcription Factor 6RUNX2medicine.anatomical_structureBiochemistryGene Expression Regulation030220 oncology & carcinogenesisOsteocalcinbiology.proteinAlkaline phosphataseCalciumQuercetinSignal transductionBiochemical pharmacology
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TP53 and p16INK4A, but not H-KI-Ras, are involved in tumorigenesis and progression of pleomorphic adenomas.

2006

The putative role of TP53 and p16INK4A tumor suppressor genes and Ras oncogenes in the development and progression of salivary gland neoplasias was studied in 28 cases of pleomorphic adenomas (PA), 4 cases of cystic adenocarcinomas, and 1 case of carcinoma ex-PA. Genetic and epigenetic alterations in the above genes were analyzed by Polymerase Chain Reaction/Single Strand Conformational Polymorphism (PCR/SSCP) and sequencing and by Methylation Specific-PCR (MS-PCR). Mutations in TP53 were found in 14% (4/28) of PAs and in 60% (3/5) of carcinomas. Mutations in H-Ras and K-Ras were identified in4%(1/28) and7% (2/28) of PAs, respectively. Only 20% (1/5) of carcinomas screened displayed mutatio…

AdenomaAdenomaGenotypePhysiologyClinical BiochemistryBiologymedicine.disease_causeMethylationEpigenesis GeneticProto-Oncogene Proteins p21(ras)GenotypemedicineCarcinomaHumansEpigeneticsTP53GeneCyclin-Dependent Kinase Inhibitor p16Base SequenceSingle-strand conformation polymorphismCell BiologyMethylationmedicine.diseaseMolecular biologyCell Transformation NeoplasticMutationDisease ProgressionTumor Suppressor Protein p53Carcinogenesis
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Colonoscopy and reduction of colorectal cancer risk by molecular tumor subtypes: a population-based case-control study

2020

AbstractObjectiveIn previous studies, the protective effect of colonoscopy was generally stronger for distal than for proximal colorectal cancer (CRC). This study aimed to investigate whether the association of colonoscopy and CRC risk varies according to major molecular pathological features and pathways of CRC.DesignPopulation-based case-control study from Germany, including 2132 patients with a first diagnosis of CRC and information on major molecular tumor markers, and 2486 control participants without CRC. Detailed participant characteristics were collected by standardized questionnaires and information on previous colonoscopy was derived from medical records. Polytomous logistic regre…

AdenomaMaleProto-Oncogene Proteins B-rafOncologymedicine.medical_specialtyColorectal cancerPopulationRectumColonoscopymedicine.disease_cause03 medical and health sciences0302 clinical medicineGermanyInternal medicineBiomarkers TumormedicineHumanseducationneoplasmsAgedAged 80 and overeducation.field_of_studyHepatologyCpG Island Methylator Phenotypemedicine.diagnostic_testbusiness.industryGastroenterologyCase-control studyCancerColonoscopyOdds ratioDNA MethylationMiddle Agedmedicine.diseaseConfidence intervaldigestive system diseasesmedicine.anatomical_structureCase-Control Studies030220 oncology & carcinogenesisMutationCpG IslandsFemaleMicrosatellite Instability030211 gastroenterology & hepatologyObservational studyKRASColorectal Neoplasmsbusiness
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Novel mutations of the MET proto-oncogene in papillary renal carcinomas.

1999

Hereditary papillary renal carcinoma (HPRC) is characterized by multiple, bilateral papillary renal carcinomas. Previously, we demonstrated missense mutations in the tyrosine kinase domain of the MET proto-oncogene in HPRC and a subset of sporadic papillary renal carcinomas. In this study, we screened a large panel of sporadic papillary renal carcinomas and various solid tumors for mutations in the MET proto-oncogene. Summarizing these and previous results, mutations of the MET proto-oncogene were detected in 17/129 sporadic papillary renal carcinomas but not in other solid tumors. We detected five novel missense mutations; three of five mutations were located in the ATP-binding region of t…

AdenomaModels MolecularCancer ResearchProtein ConformationDNA Mutational AnalysisMolecular Sequence DataHereditary Papillary Renal Cell CarcinomaBiologymedicine.disease_causeTransfectionProto-Oncogene MasReceptor tyrosine kinaseMiceAdenosine TriphosphateNeoplastic Syndromes HereditaryProto-OncogenesGeneticsCarcinomamedicineMissense mutationAnimalsHumansPoint MutationAmino Acid SequencePhosphorylationCodonMolecular BiologyKidneyMutationBinding SitesSequence Homology Amino AcidPoint mutation3T3 CellsDNA NeoplasmProto-Oncogene Proteins c-metmedicine.diseaseCarcinoma PapillaryKidney NeoplasmsNeoplasm Proteinsmedicine.anatomical_structureCell Transformation NeoplasticCancer researchbiology.proteinMutagenesis Site-DirectedTyrosine kinaseProtein Processing Post-TranslationalSequence AlignmentOncogene
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Coexpression of IL-6 and soluble IL-6R causes nodular regenerative hyperplasia and adenomas of the liver

1998

Studies with tumor necrosis factor p55 receptor- and interleukin-6 (IL-6)-deficient mice have shown that IL-6 is required for hepatocyte proliferation and reconstitution of the liver mass after partial hepatectomy. The biological activities of IL-6 are potentiated when this cytokine binds soluble forms of its specific receptor subunit (sIL-6R) and the resulting complex interacts with the transmembrane signaling chain gp130. We show here that double transgenic mice expressing high levels of both human IL-6 and sIL-6R under the control of liver-specific promoters spontaneously develop nodules of hepatocellular hyperplasia around periportal spaces and present signs of sustained hepatocyte prol…

AdenomaSTAT3 Transcription FactorAdenomail-6; liver adenomas; nodular hyperplasia; soluble il-6rMice TransgenicBiologyGeneral Biochemistry Genetics and Molecular BiologyProto-Oncogene Proteins c-mycMiceMyeloproliferative Disordersil-6medicineAnimalsnodular hyperplasiaReceptorMolecular BiologyHyperplasialiver adenomasHaptoglobinsGeneral Immunology and MicrobiologyInterleukin-6General NeuroscienceLiver NeoplasmsHyperplasiaGlycoprotein 130medicine.diseaseReceptors Interleukin-6Liver regenerationLiver RegenerationDNA-Binding Proteinsmedicine.anatomical_structureGene Expression RegulationLiverSolubilityHepatocyteTrans-ActivatorsCancer researchEndothelium Vascularsoluble il-6rNodular regenerative hyperplasiaResearch ArticleThe EMBO Journal
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