Search results for "TRANSCRIPTION"

showing 10 items of 2278 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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Post-transcriptional, post-translational and pharmacological regulation of tissue factor pathway inhibitor.

2018

: Tissue factor (TF) pathway inhibitor (TFPI) is an endogenous natural anticoagulant that readily inhibits the extrinsic coagulation initiation complex (TF-FVIIa-Xa) and prothrombinase (FXa, FVa and calcium ions). Alternatively, spliced TFPI isoforms (α, β and δ) are expressed by vascular and extravascular cells and regulate thrombosis and haemostasis, as well as cell signalling functions of TF complexes via protease-activated receptors (PARs). Proteolysis of TFPI plays an important role in regulating physiological roles of the TF pathway in host defense and possibly haemostasis. Elimination of TFPI inhibition has therefore been proposed as an approach to improve haemostasis in haemophilia …

0301 basic medicineProteasesCell signalingProteolysisLipoproteinsEndogeny030204 cardiovascular system & hematology03 medical and health sciencesTissue factor0302 clinical medicineTissue factor pathway inhibitorProthrombinasemedicineAnimalsHumansRNA Processing Post-TranscriptionalReceptorHemostasismedicine.diagnostic_testChemistryThrombosisHematologyGeneral MedicineCell biology030104 developmental biologyProtein Processing Post-TranslationalBlood coagulationfibrinolysis : an international journal in haemostasis and thrombosis
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BAG3 regulates total MAP1LC3B protein levels through a translational but not transcriptional mechanism

2015

Autophagy is mainly regulated by post-translational and lipid modifications of ATG proteins. In some scenarios, the induction of autophagy is accompanied by increased levels of certain ATG mRNAs such as MAP1LC3B/LC3B, ATG5 or ATG12. However, little is known about the regulation of ATG protein synthesis at the translational level. The cochaperone of the HSP70 system BAG3 (BCL2-associated athanogene 3) has been associated to LC3B lipidation through an unknown mechanism. In the present work, we studied how BAG3 controls autophagy in HeLa and HEK293 cells. Our results showed that BAG3 regulates the basal amount of total cellular LC3B protein by controlling its mRNA translation. This effect was …

0301 basic medicineProteasome Endopeptidase ComplexTranscription GeneticATG8ATG5BiologyBAG3ATG1203 medical and health sciences0302 clinical medicineProtein biosynthesisHumansRNA MessengerMolecular BiologyAdaptor Proteins Signal TransducingGeneticsGene knockdownAutophagyCell BiologyLipidsBasic Research PaperCell biologyHEK293 Cells030104 developmental biologyProtein BiosynthesisProteolysisApoptosis Regulatory ProteinsLysosomesMicrotubule-Associated ProteinsMAP1LC3B030217 neurology & neurosurgeryHeLa 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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Metabolites related to purine catabolism and risk of type 2 diabetes incidence; modifying effects of the TCF7L2-rs7903146 polymorphism

2019

Studies examining associations between purine metabolites and type 2 diabetes (T2D) are limited. We prospectively examined associations between plasma levels of purine metabolites with T2D risk and the modifying effects of transcription factor-7-like-2 (TCF7L2) rs7903146 polymorphism on these associations. This is a case-cohort design study within the PREDIMED study, with 251 incident T2D cases and a random sample of 694 participants (641 non-cases and 53 overlapping cases) without T2D at baseline (median follow-up: 3.8 years). Metabolites were semi-quantitatively profiled with LC-MS/MS. Cox regression analysis revealed that high plasma allantoin levels, including allantoin-to-uric acid rat…

0301 basic medicinePurineMalePolymorphism (Crystallography)endocrine system diseaseslcsh:MedicineType 2 diabetesDiabetis no-insulinodependentchemistry.chemical_compound0302 clinical medicineBlood plasmaMetabolitesNon-insulin-dependent diabetesProspective Studieslcsh:ScienceMultidisciplinaryDiabetisIncidencePrognosisMetabòlits3. Good healthMetabolomeFemaleTranscription Factor 7-Like 2 Proteinmedicine.drugmedicine.medical_specialtyendocrine systemPolymorphism Single NucleotideArticle03 medical and health sciencesAllantoin:Ciencias de la Salud::Medicina preventiva [Materias Investigacion]Diabetes mellitusInternal medicinemedicineHumansGenetic Predisposition to DiseaseInosineAgedbusiness.industrylcsh:Rnutritional and metabolic diseasesPolimorfisme (Cristal·lografia)Xanthinemedicine.disease030104 developmental biologyEndocrinologychemistryDiabetes Mellitus Type 2PurinesSpainCase-Control Studieslcsh:QbusinessTCF7L2030217 neurology & neurosurgeryBiomarkersFollow-Up Studies
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Metabolic and inflammatory reprogramming of macrophages by ONC201 translates in a pro-inflammatory environment even in presence of glioblastoma cells

2020

Tumor-associated macrophages facilitate tumor progression and resistance to therapy. Their capacity for metabolic and inflammatory reprogramming represents an attractive therapeutic target. ONC201/TIC10 is an anticancer molecule that antagonizes the dopamine receptor D2 and affects mitochondria integrity in tumor cells. We examined whether ONC201 induces a metabolic and pro-inflammatory switch in primary human monocyte-derived macrophages that reactivates their antitumor activities, thus enhancing the onco-toxicity of ONC201. Contrary to glioblastoma cells, macrophages exhibited a low ratio of dopamine receptors D2/D5 gene expression and were resistant to ONC201 cytotoxicity. Macrophages re…

0301 basic medicinePyridinesImmunology610 MedizinGlutamic AcidAntineoplastic AgentsMitochondrionBiology570 Life sciences03 medical and health sciences0302 clinical medicineImmune systemCell Line TumorDopamine receptor D2610 Medical sciencesTumor MicroenvironmentHumansImmunology and AllergyMacrophageReceptors Dopamine D5Tumor microenvironmentReceptors Dopamine D2MacrophagesImidazolesMitochondriaCell biologyGene Expression Regulation NeoplasticPyrimidines030104 developmental biologyDrug Resistance NeoplasmTumor progressionDopamine receptorEnergy MetabolismGlioblastomaReprogrammingTranscription Factor CHOPSignal Transduction030215 immunology570 Biowissenschaften
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Regulatory network analysis in estradiol-treated human endothelial cells.

2021

Background/Aims: Estrogen has been reported to have beneficial effects on vascular biology through direct actions on endothelium. Together with transcription factors, miRNAs are the major drivers of gene expression and signaling networks. The objective of this study was to identify a com-prehensive regulatory network (miRNA-transcription factor-downstream genes) that controls the transcriptomic changes observed in endothelial cells exposed to estradiol. Methods: miR-NA/mRNA interactions were assembled using our previous microarray data of human umbilical vein endothelial cells (HUVEC) treated with 17ß- Estradiol (E2) (1 nmol/lL, 24 h). miRNA--mRNA pairings and their associated canonical pat…

0301 basic medicineQH301-705.5FisiologiaBiologyCatalysisArticleInorganic Chemistry03 medical and health sciences0302 clinical medicineGene expressionCadherin bindingHuman Umbilical Vein Endothelial CellsHumansGene Regulatory NetworksRNA MessengerPhysical and Theoretical ChemistryBiology (General)Molecular BiologyTranscription factorQD1-999Spectroscopytranscription factormiRNAEstradiolMicroarray analysis techniquesOrganic ChemistryPromoterEstrogensGeneral Medicineendothelial cellsComputer Science ApplicationsCell biologyDNA binding siteChemistryMicroRNAs030104 developmental biology030220 oncology & carcinogenesisCell adhesion molecule bindingTRANSFACTranscriptome
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Eukaryotic RNA Polymerases: The Many Ways to Transcribe a Gene

2021

In eukaryotic cells, three nuclear RNA polymerases (RNA pols) carry out the transcription from DNA to RNA, and they all seem to have evolved from a single enzyme present in the common ancestor with archaea. The multiplicity of eukaryotic RNA pols allows each one to remain specialized in the synthesis of a subset of transcripts, which are different in the function, length, cell abundance, diversity, and promoter organization of the corresponding genes. We hypothesize that this specialization of RNA pols has conditioned the evolution of the regulatory mechanisms used to transcribe each gene subset to cope with environmental changes. We herein present the example of the homeostatic regulation …

0301 basic medicineQH301-705.5Mini ReviewRNA polymerase IIBiochemistry Genetics and Molecular Biology (miscellaneous)BiochemistryRNA polymerase III03 medical and health sciencesRNA pol III0302 clinical medicineTranscription (biology)evolutionRNA polymerase IMolecular BiosciencesRNA pol IBiology (General)Molecular BiologyGenePolymeraseGeneticsMessenger RNAbiologyCèl·lules eucariotesnucleusRNARNA pol II030104 developmental biologybiology.proteinRNAtranscription030217 neurology & neurosurgeryFrontiers in Molecular Biosciences
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Rpb1 foot mutations demonstrate a major role of Rpb4 in mRNA stability during stress situations in yeast.

2016

The RPB1 mutants in the foot region of RNA polymerase II affect the assembly of the complex by altering the correct association of both the Rpb6 and the Rpb4/7 dimer. Assembly defects alter both transcriptional activity as well as the amount of enzyme associated with genes. Here, we show that the global transcriptional analysis of foot mutants reveals the activation of an environmental stress response (ESR), which occurs at a permissive temperature under optimal growth conditions. Our data indicate that the ESR that occurs in foot mutants depends mostly on a global post-transcriptional regulation mechanism which, in turn, depends on Rpb4-mRNA imprinting. Under optimal growth conditions, we …

0301 basic medicineRNA StabilitySaccharomyces cerevisiae ProteinsTranscription GeneticRNA StabilityMutantSaccharomyces cerevisiaeBiophysicsRNA polymerase IISaccharomyces cerevisiaeBiochemistryMolecular Imprinting03 medical and health sciencesStructural BiologyTranscription (biology)Stress PhysiologicalGeneticsRNA MessengerImprinting (psychology)Molecular BiologyGeneGeneticsMessenger RNAbiologybiology.organism_classificationCell biology030104 developmental biologyMutationbiology.proteinRNA Polymerase IIBiochimica et biophysica acta
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Growth rate controls mRNA turnover in steady and non-steady states.

2016

Gene expression has been investigated in relation with growth rate in the yeast Saccharomyces cerevisiae, following different experimental strategies. The expression of some specific gene functional categories increases or decreases with growth rate. Our recently published results have unveiled that these changes in mRNA concentration with growth depend on the relative alteration of mRNA synthesis and decay, and that, in addition to this gene-specific transcriptomic signature of growth, global mRNA turnover increases with growth rate. We discuss here these results in relation with other previous and concurrent publications, and we add new evidence which indicates that growth rate controls m…

0301 basic medicineRNA StabilitySaccharomyces cerevisiaeSaccharomyces cerevisiaeyeastTranscriptome03 medical and health sciencesTranscription (biology)Gene Expression Regulation FungalGene expressionmRNA stabilityGrowth rateRNA MessengerMolecular BiologyGenePoint of ViewMessenger RNAbiologyRNA FungalCell Biologybiology.organism_classificationMolecular biologyYeastCell biology030104 developmental biologygrowth rateGene expressiontranscriptionRNA biology
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