Search results for "Oncogene"

showing 10 items of 1005 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
researchProduct

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
researchProduct

The role of extracellular calcium in bone metastasis

2016

AbstractThis review summarizes the role of extracellular calcium, as found present in the bone tissue, in the process of bone metastasis.

0301 basic medicinelcsh:Diseases of the musculoskeletal systemIGF insulin-like growth factorPGE-2 prostaglandin E-2Bone tissueFibroblast growth factorM-CSF macrophage colony-stimulating factorPDGF platelet-derived growth factorBone remodelingSK3 small conductance calcium-activated potassium channel 30302 clinical medicineERK extracellular signal-regulated kinaseTGFβ transforming growth factor betaBMP's bone morphogenetic proteinsbiologyAKT AKT8 virus oncogene cellular homologBone metastasislcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenshumanitiescAMP cyclic adenosine monophosphatemedicine.anatomical_structureOncologyRANKL030220 oncology & carcinogenesisIon channelsCaSR calcium-sensing receptorPTHrP parathyroid hormone-related proteinPlatelet-derived growth factor receptorResearch PaperTRP transient receptor potentialmedicine.medical_specialtychemistry.chemical_elementCalciumRANKL receptor activator of NF-κB ligandlcsh:RC254-28203 medical and health sciencesPLC phospholipase CInternal medicinemedicineExtracellularCaSRET-1 endothelin-1PTEN phosphatase and tensin homolog deleted on chromosome 10business.industryBone metastasismedicine.diseaseFGF fibroblast growth factor030104 developmental biologyEndocrinologyPSA prostate specific antigenchemistryCOPD chronic obstructive pulmonary diseasebiology.proteinCancer researchJNK jun N-terminal kinasePKA protein kinase ARANK receptor activator of NF-κBCalciumlcsh:RC925-935businessMAPK mitogen-activated protein kinaseJournal of Bone Oncology
researchProduct

ROS and Lipid Droplet accumulation induced by high glucose exposure in healthy colon and Colorectal Cancer Stem Cells

2020

Lipid Droplets (LDs) are emerging as crucial players in colon cancer development and maintenance. Their expression has been associated with high tumorigenicity in Cancer Stem Cells (CSCs), so that they have been proposed as a new functional marker in Colorectal Cancer Stem Cells (CR-CSCs). They are also indirectly involved in the modulation of the tumor microenvironment through the production of pro-inflammatory molecules. There is growing evidence that a possible connection between metabolic alterations and malignant transformation exists, although the effects of nutrients, primarily glucose, on the CSC behavior are still mostly unexplored. Glucose is an essential fuel for cancer cells, an…

0301 basic medicinelcsh:QH426-470Colorectal cancerColorectal cancer stem cellsSettore MED/50 - Scienze Tecniche Mediche ApplicateLipid dropletBiochemistryMalignant transformation03 medical and health sciences0302 clinical medicineCancer stem cellLipid dropletFull Length ArticlemedicineCholesterol metabolismMolecular BiologyOncogeneGenetics (clinical)PI3K/AKT/mTOR pathwaySettore MED/04 - Patologia Generalelcsh:R5-920Tumor microenvironmentChemistryPI3K-AKTColorectal cancer stem cellCell BiologyOncogenesmedicine.diseaseLipid droplets3. Good healthlcsh:GeneticsSettore BIO/12 - Biochimica Clinica E Biologia Molecolare Clinica030104 developmental biologyOxidative stress030220 oncology & carcinogenesisFatty acid metabolismCancer cellCancer researchOxidative streSettore MED/46 - Scienze Tecniche Di Medicina Di LaboratorioStem cellHigh glucoselcsh:Medicine (General)Genes & Diseases
researchProduct

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
researchProduct

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
researchProduct

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
researchProduct

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
researchProduct

Genomic and non-genomic mechanisms of action of thyroid hormones and their catabolite 3,5-diiodo-l-thyronine in Mammals

2020

Since the realization that the cellular homologs of a gene found in the retrovirus that contributes to erythroblastosis in birds (v-erbA), i.e. the proto-oncogene c-erbA encodes the nuclear receptors for thyroid hormones (THs), most of the interest for THs focalized on their ability to control gene transcription. It was found, indeed, that, by regulating gene expression in many tissues, these hormones could mediate critical events both in development and in adult organisms. Among their effects, much attention was given to their ability to increase energy expenditure, and they were early proposed as anti-obesity drugs. However, their clinical use has been strongly challenged by the concomita…

0301 basic medicinenonalcoholic fatty liver diseaseobesityDiiodothyroninesEndogenyReviewthyroid hormone metabolism and transportMitochondrionmedicine.disease_causeProto-Oncogene Maslcsh:Chemistry0302 clinical medicineTranscription (biology)Settore BIO/10 - BiochimicaGene expressionSettore BIO/06 - Anatomia Comparata E CitologiaSettore MED/49 - Scienze Tecniche Dietetiche Applicatelcsh:QH301-705.5SpectroscopyMammalsReceptors Thyroid Hormonehepatic steatosisthyroid hormone mechanisms of actionGeneral Medicineresistance to thyroid hormones (RTH)Computer Science ApplicationsCell biology35-diiodo-L-thyronineThyroid Hormones030209 endocrinology & metabolismBiologyIodide PeroxidaseCatalysisInorganic Chemistry03 medical and health sciencesmedicineAnimalsHumansPhysical and Theoretical ChemistryMolecular BiologyGeneOrganic ChemistryBiological TransportLipid Metabolismhepatic steatosi030104 developmental biologyNuclear receptorlcsh:Biology (General)lcsh:QD1-999MutationBasal MetabolismLipid PeroxidationOxidative stressHormone
researchProduct

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
researchProduct