Search results for "Proto-oncogene proteins"

showing 10 items of 698 documents

Structural and mechanistic insights into the interaction of the circadian transcription factor BMAL1 with the KIX domain of the CREB-binding protein

2019

JBC papers in press xx, 16604-16619 (2019). doi:10.1074/jbc.RA119.009845

0301 basic medicineendocrine systemCircadian clockTranscription factor complex610BiochemistryProtein Structure SecondaryProtein–protein interaction03 medical and health sciencesTransactivationMiceProto-Oncogene Proteins c-mybProtein DomainsX-Ray DiffractionCircadian ClocksScattering Small AngleAnimalsddc:610Amino Acid SequenceCREB-binding proteinMolecular BiologyTernary complexTranscription factorBinding Sites030102 biochemistry & molecular biologybiologyChemistryARNTL Transcription FactorsCell BiologyHistone-Lysine N-MethyltransferaseSurface Plasmon ResonanceCREB-Binding ProteinRecombinant ProteinsCell biologyProtein Structure Tertiary030104 developmental biologyStructural biologyProtein Structure and Foldingbiology.proteinMutagenesis Site-DirectedMyeloid-Lymphoid Leukemia ProteinProtein Binding
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Evidence That Graves' Ophthalmopathy Immunoglobulins Do Not Directly Activate IGF-1 Receptors

2018

Background: Graves' ophthalmopathy (GO) pathogenesis involves thyrotropin (TSH) receptor (TSHR)-stimulating autoantibodies. Whether there are autoantibodies that directly stimulate insulin-like growth factor 1 receptors (IGF-1Rs), stimulating insulin-like growth factor receptor antibodies (IGFRAbs), remains controversial. This study attempted to determine whether there are stimulating IGFRAbs in patients with GO. Methods: Immunoglobulins (Igs) were purified from normal volunteers (NV-Igs) and patients with GO (GO-Igs). The effects of TSH, IGF-1, NV-Igs, and GO-Igs on pAKT and pERK1/2, members of pathways used by IGF-1R and TSHR, were compared in orbital fibroblasts from GO patients (GOFs) a…

0301 basic medicineendocrine systemendocrine system diseasesEndocrinology Diabetes and MetabolismImmunoglobulins030209 endocrinology & metabolismCell LineReceptor IGF Type 1PathogenesisGraves' ophthalmopathy03 medical and health sciences0302 clinical medicineEndocrinologymedicineHumansImmunology Autoimmunity and Graves' OphthalmopathyPhosphorylationReceptorbiologybusiness.industryAutoantibodyReceptors Thyrotropinmedicine.diseaseeye diseasesGraves Ophthalmopathy030104 developmental biologyImmunologybiology.proteinlipids (amino acids peptides and proteins)AntibodybusinessProto-Oncogene Proteins c-akthormones hormone substitutes and hormone antagonists
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Loss of c-Met signaling sensitizes hepatocytes to lipotoxicity and induces cholestatic liver damage by aggravating oxidative stress.

2016

Recent studies confirmed a critical importance of c-Met signaling for liver regeneration by modulating redox balance. Here we used liver-specific conditional knockout mice (MetKO) and a nutritional model of hepatic steatosis to address the role of c-Met in cholesterol-mediated liver toxicity. Liver injury was assessed by histopathology and plasma enzymes levels. Global transcriptomic changes were examined by gene expression microarray, and key molecules involved in liver damage and lipid homeostasis were evaluated by Western blotting. Loss of c-Met signaling amplified the extent of liver injury in MetKO mice fed with high-cholesterol diet for 30days as evidenced by upregulation of liver enz…

0301 basic medicinemedicine.medical_specialtyCell SurvivalCholestasis IntrahepaticBiologyToxicologymedicine.disease_causeArticleCholesterol Dietary03 medical and health sciencesMice0302 clinical medicineLiver Function TestsInternal medicinemedicineAnimalsLiver X receptorLiver injuryMice Knockoutmedicine.diagnostic_testLipid metabolismProto-Oncogene Proteins c-metmedicine.diseaseLipid MetabolismGlutathioneLipidsLiver regenerationOxidative Stress030104 developmental biologyEndocrinologyLipotoxicity030220 oncology & carcinogenesisHepatocytesLipid PeroxidationSteatosisLiver function testsOxidative stressSignal TransductionToxicology
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Short Term Palmitate Supply Impairs Intestinal Insulin Signaling via Ceramide Production

2016

International audience; The worldwide prevalence of metabolic diseases is increasing, and there are global recommendations to limit consumption of certain nutrients, especially saturated lipids. Insulin resistance, a common trait occurring in obesity and type 2 diabetes, is associated with intestinal lipoprotein overproduction. However, the mechanisms by which the intestine develops insulin resistance in response to lipid overload remain unknown. Here, we show that insulin inhibits triglyceride secretion and intestinal microsomal triglyceride transfer protein expression in vivo in healthy mice force-fed monounsaturated fatty acid-rich olive oil but not in mice force-fed saturated fatty acid…

0301 basic medicinemedicine.medical_specialtyCeramidemedicine.medical_treatmentPalmitic Acid[SDV.BC]Life Sciences [q-bio]/Cellular BiologyPalm OilCeramidesBiochemistryPalmitic acidMice03 medical and health scienceschemistry.chemical_compoundInsulin resistance[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyInternal medicinemedicineAnimalsHumansInsulinPlant OilsIntestinal MucosaPhosphorylationMolecular BiologyComputingMilieux_MISCELLANEOUS2. Zero hungerbiologyTriglycerideInsulinCell BiologyLipid signalingmedicine.diseaseLipids3. Good healthInsulin receptorEnterocytes030104 developmental biologyEndocrinologychemistrySaturated fatty acidbiology.proteinCaco-2 CellsProto-Oncogene Proteins c-akt[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologySignal TransductionJournal of Biological Chemistry
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Hepatic B cell leukemia-3 promotes hepatic steatosis and inflammation through insulin-sensitive metabolic transcription factors.

2016

Background & Aims The pathomechanisms underlying non-alcoholic fatty liver disease (NAFLD) and the involved molecular regulators are incompletely explored. The nuclear factor-kappa B (NF-κB)-cofactor gene B cell leukemia-3 ( Bcl-3 ) plays a critical role in altering the transcriptional capacity of NF-κB – a key inducer of inflammation – but also of genes involved in cellular energy metabolism. Methods To define the role of Bcl-3 in non-alcoholic steatohepatitis (NASH), we developed a novel transgenic mouse model with hepatocyte-specific overexpression of Bcl-3 ( Bcl-3 Hep ) and employed a high-fat, high-carbohydrate dietary feeding model. To characterize the transgenic model, deep RNA seque…

0301 basic medicinemedicine.medical_specialtyCirrhosisCarcinoma Hepatocellularmedicine.medical_treatmentBiology03 medical and health sciencesLiver diseaseMice0302 clinical medicineB-Cell Lymphoma 3 ProteinInternal medicineProto-Oncogene ProteinsmedicineAnimalsHumansInsulinInflammationHepatologyInsulinLiver cellFatty liverLiver Neoplasmsmedicine.disease030104 developmental biologyEndocrinology030220 oncology & carcinogenesisLipogenesisSteatohepatitisSteatosisTranscription FactorsJournal of hepatology
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Roles of NGAL and MMP-9 in the tumor microenvironment and sensitivity to targeted therapy.

2016

Various, diverse molecules contribute to the tumor microenvironment and influence invasion and metastasis. In this review, the roles of neutrophil gelatinase-associated lipocalin (NGAL) and matrix metalloproteinase-9 (MMP-9) in the tumor microenvironment and sensitivity to therapy will be discussed. The lipocalin family of proteins has many important functions. For example when NGAL forms a complex with MMP-9 it increases its stability which is important in cancer metastasis. Small hydrophobic molecules are bound by NGAL which can alter their entry into and efflux from cells. Iron transport and storage are also influenced by NGAL activity. Regulation of iron levels is important for survival…

0301 basic medicinemedicine.medical_treatmentDrug resistance; Iron transport; Lcn2; Lipocalins; MMP-9; NGAL; SiderocalinsAcute-Phase ProteinLipocalinLipocalinMetastasisTargeted therapyAntineoplastic Agent0302 clinical medicineNeoplasmsTumor MicroenvironmentNeoplasm MetastasisNGALProto-Oncogene ProteinMedicine (all)SiderocalinsLipocalinsNeoplasm MetastasiMatrix Metalloproteinase 9030220 oncology & carcinogenesismedicine.symptomSignal transductionMMP-9HumanProtein BindingSignal TransductionSiderocalinAntineoplastic AgentsInflammationBiologyModels Biological03 medical and health sciencesLcn2Lipocalin-2Proto-Oncogene ProteinsmedicineHumansIron transportMolecular BiologyTumor microenvironmentInnate immune systemCell Biologymedicine.disease030104 developmental biologyDrug resistanceCancer cellImmunologyCancer researchNeoplasmAcute-Phase Proteins
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Designer Thiopurine-analogues for Optimised Immunosuppression in Inflammatory Bowel Diseases.

2015

Background and Aims: The clinical use of azathioprine and 6-mercaptopurine is limited by their delayed onset of action and potential side effects such as myelosuppression and hepatotoxicity. As these drugs specifically target the Vav1/Rac1 signalling pathway in T lamina propria lymphocytes via their metabolite 6-thio-GTP, we studied expression and optimised suppression of this pathway in inflammatory bowel diseases [IBD]. Methods: Rac1 and Vav1 expressions were analysed in mucosal immune cells in IBD patients. Targeted molecular modelling of the 6-thio-GTP molecule was performed to optimise Rac1 blockade; 44 modified designer thiopurine-analogues were tested for apoptosis induction, potenti…

0301 basic medicinerac1 GTP-Binding Proteinmedicine.medical_treatmentT-LymphocytesAzathioprineApoptosisInflammatory bowel diseaseDesigner Drugs03 medical and health sciences0302 clinical medicineImmune systemIntestinal mucosamedicineHumansIntestinal MucosaProto-Oncogene Proteins c-vavLamina propriaThiopurine methyltransferasebiologybusiness.industryMercaptopurineGastroenterologyImmunosuppressionGeneral Medicinemedicine.diseaseInflammatory Bowel Diseases030104 developmental biologymedicine.anatomical_structureApoptosisCase-Control StudiesDrug DesignImmunologybiology.protein030211 gastroenterology & hepatologybusinessBiomarkersImmunosuppressive Agentsmedicine.drugSignal TransductionJournal of Crohn'scolitis
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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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