Search results for "Transcription"

showing 10 items of 2278 documents

Bainbridge-Ropers syndrome caused by loss-of-function variants in ASXL3: a recognizable condition

2016

International audience; Truncating ASXL3 mutations were first identified in 2013 by Bainbridge et al. as a cause of syndromic intellectual disability in four children with similar phenotypes using whole-exome sequencing. The clinical features - postulated by Bainbridge et al. to be overlapping with Bohring-Opitz syndrome - were developmental delay, severe feeding difficulties, failure to thrive and neurological abnormalities. This condition was included in OMIM as 'Bainbridge-Ropers syndrome' (BRPS, #615485). To date, a total of nine individuals with BRPS have been published in the literature in four reports (Bainbridge et al., Dinwiddie et al, Srivastava et al. and Hori et al.). In this re…

Male0301 basic medicinemedicine.medical_specialtyMicrocephalyfamilyAdolescentphenotypeDevelopmental DisabilitiesSevere muscular hypotoniaMedizinTrigonocephaly030105 genetics & heredityBiologyArticle03 medical and health sciencesIntellectual disabilityGeneticsmedicineHumansCraniofacial[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsnovo frameshift mutationgenedisordersGenetics (clinical)GeneticsInfantSyndromemedicine.diseaseDermatologyFailure to Thrive030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsintellectual disabilityChild Preschoolbohring-opitz syndromeMutationFailure to thriveMedical geneticsFemalemedicine.symptomBohring–Opitz syndromeTranscription Factors
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Neuropeptide FF increases M2 activation and self-renewal of adipose tissue macrophages

2017

The quantity and activation state of adipose tissue macrophages (ATMs) impact the development of obesity-induced metabolic diseases. Appetite-controlling hormones play key roles in obesity; however, our understanding of their effects on ATMs is limited. Here, we have shown that human and mouse ATMs express NPFFR2, a receptor for the appetite-reducing neuropeptide FF (NPFF), and that NPFFR2 expression is upregulated by IL-4, an M2-polarizing cytokine. Plasma levels of NPFF decreased in obese patients and high-fat diet-fed mice and increased following caloric restriction. NPFF promoted M2 activation and increased the proliferation of murine and human ATMs. Both M2 activation and increased ATM…

Male0301 basic medicinemedicine.medical_specialty[SDV.BIO]Life Sciences [q-bio]/BiotechnologyUbiquitin-Protein LigasesAdipose tissue macrophagesMafB Transcription FactorAdipose tissueMice TransgenicReceptors Cell SurfaceSelf renewalMice03 medical and health sciencesClinical investigationInternal medicinemedicineAnimalsNeuropeptide FFTranscription factorAdaptor Proteins Signal TransducingCell ProliferationSTAT62. Zero hungerArginasebiologybusiness.industryChemistryMacrophagesProteinsSciences du Vivant [q-bio]/BiotechnologiesGeneral MedicineMacrophage ActivationInterleukin-10Ubiquitin ligaseCell biologyEndocrinology030104 developmental biologyAdipose TissueMAFBbiology.proteinInterleukin-4CorrigendumbusinessOligopeptidesMacrophage proliferationResearch ArticleJournal of Clinical Investigation
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Poor transcript-protein correlation in the brain: negatively correlating gene products reveal neuronal polarity as a potential cause

2018

Transcription, translation, and turnover of transcripts and proteins are essential for cellular function. The contribution of those factors to protein levels is under debate, as transcript levels and cognate protein levels do not necessarily correlate due to regulation of translation and protein turnover. Here we propose neuronal polarity as a third factor that is particularly evident in the CNS, leading to considerable distances between somata and axon terminals. Consequently, transcript levels may negatively correlate with cognate protein levels in CNS regions, i.e., transcript and protein levels behave reciprocally. To test this hypothesis, we performed an integrative inter-omics study a…

Male0301 basic medicineneuronal polarityintegrative omics[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyBiologynegative transcript|protein correlationProteomicsBiochemistryRats Sprague-DawleyTranscriptome03 medical and health sciencesCellular and Molecular Neurosciencetranscriptomics0302 clinical medicineproteomicsTranscription (biology)[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]AnimalsRNA MessengerGeneNeuronsProtein turnoverBrainCell PolarityProteinsRatsTransport proteinCell biology030104 developmental biologySuperior olivary complexprotein transportFemaleDNA microarray030217 neurology & neurosurgery
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Induction of the peroxisome proliferator activated receptor by fenofibrate in rat liver

1992

AbstractThe process of peroxisome proliferation in rodent liver by hypolipidemic compounds and related substances has recently been shown to be receptor-madiated. In the present study, we have examined the effect of oral administration of the strong peroxisome proliferator fenofibrate on the hepatic expression level of the peroxisome proliferator activated receptor (PPAR) in rats. Immunoblots of rat liver cytosols and nuclear extracs using antibodies raised against recombinant PPAR/β-galactosidase fusion proteins revealed a pronounced increase in the amount of PPAR protein in response to fenofibrate treatment. This induction could also be confirmed at the level or RNA by Northern blotting. …

Male1303 BiochemistryReceptors Cytoplasmic and Nuclear10050 Institute of Pharmacology and ToxicologyPeroxisome proliferator-activated receptorPPARMicrobodiesPolymerase Chain ReactionBiochemistryPPAR agonist1307 Cell BiologyMiceCytosol1315 Structural BiologyFenofibrateStructural Biologychemistry.chemical_classificationMice Inbred BALB CFenofibrateOligodeoxyribonucleotidesPeroxisome proliferator-activated receptor alphaFusion proteinmedicine.drugmedicine.medical_specialtyPeroxisome proliferator-activated receptor gammamRNAMolecular Sequence DataBiophysicsPeroxisome ProliferationReceptors Cell Surface610 Medicine & healthBiology1311 GeneticsInternal medicine1312 Molecular BiologyGeneticsmedicineAnimalsNorthern blotMolecular BiologyAntibodyHypolipidemic compoundCell NucleusMessenger RNABase SequenceImmune SeraCell BiologyBlotting NorthernRatsMice Inbred C57BLEndocrinologychemistry570 Life sciences; biologyTranscription Factors1304 BiophysicsFEBS Letters
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Deregulation of ARID1A, CDH1, cMET and PIK3CA and target-related microRNA expression in gastric cancer.

2015

Genetic and epigenetic alterations play an important role in gastric cancer (GC) pathogenesis. Aberrations of the phosphatidylinositol-3-kinase signaling pathway are well described. However, emerging genes have been described such as, the chromatin remodeling gene ARID1A. Our aim was to determine the expression levels of four GC-related genes, ARID1A, CDH1, cMET and PIK3CA, and 14 target-related microRNAs (miRNAs). We compared mRNA and miRNA expression levels among 66 gastric tumor and normal adjacent mucosa samples using quantitative real-time reverse transcription PCR. Moreover, ARID1A, cMET and PIK3CA protein levels were assessed by immunohistochemistry (IHC). Finally, gene and miRNAs as…

MaleARID1AClass I Phosphatidylinositol 3-KinasesReal-Time Polymerase Chain ReactionCDH1Epigenesis GeneticPhosphatidylinositol 3-KinasesAntigens CDStomach NeoplasmsGene expressionmicroRNAmedicineBiomarkers TumorHumansRNA MessengerAgedbiologyReverse Transcriptase Polymerase Chain ReactionGene Expression Profilinggastric cancerCancerNuclear ProteinsbiomarkersMiddle AgedProto-Oncogene Proteins c-metmedicine.diseaseCadherinsMolecular biologyImmunohistochemistryChromatinGene expression profilingReverse transcription polymerase chain reactionDNA-Binding ProteinsGene Expression Regulation NeoplasticMicroRNAsReal-time polymerase chain reactionmicrorna expressionOncologyGastric Mucosabiology.proteingene expressionFemaleTranscription FactorsResearch PaperOncotarget
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Systemic blockade of ACVR2B ligands protects myocardium from acute ischemia-reperfusion injury

2019

Activin A and myostatin, members of the transforming growth factor (TGF)-β superfamily of secreted factors, are potent negative regulators of muscle growth, but their contribution to myocardial ischemia-reperfusion (IR) injury is not known. The aim of this study was to investigate if activin 2B (ACVR2B) receptor ligands contribute to myocardial IR injury. Mice were treated with soluble ACVR2B decoy receptor (ACVR2B-Fc) and subjected to myocardial ischemia followed by reperfusion for 6 or 24 h. Systemic blockade of ACVR2B ligands by ACVR2B-Fc was protective against cardiac IR injury, as evidenced by reduced infarcted area, apoptosis, and autophagy and better preserved LV systolic function fo…

MaleActivin Receptors Type IIiskemialihaksetSmad2 ProteinMyostatinPharmacologyMice0302 clinical medicineDrug DiscoverykasvutekijätMyocytes CardiacCardioprotection0303 health sciences318 Medical biotechnologybiologysydänactivins1184 Genetics developmental biology physiologyII RECEPTORS3. Good health030220 oncology & carcinogenesisMolecular MedicineOriginal ArticleSignal TransductionCardiac function curvegrowth differentiation factorsProgrammed cell deathBLOCKINGischemia-reperfusion injuryIschemiaMyocardial Reperfusion InjuryMASSta311103 medical and health sciencesMYOSTATIN-KNOCKOUTCARDIOPROTECTIONGeneticsmedicineAnimalsMolecular Biologylihassolut030304 developmental biologyPharmacologySKELETAL-MUSCLE GROWTHbusiness.industryMyocardiumFOLLISTATINMyostatinmedicine.diseaseACVR2BMice Inbred C57BLACTIVIN-AGDF11GDF11biology.protein3111 BiomedicineproteiinitbusinessReperfusion injuryDIFFERENTIATION FACTOR 11ACVR2BTranscription Factors
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Redefining the MED13L syndrome

2015

Congenital cardiac and neurodevelopmental deficits have been recently linked to the mediator complex subunit 13-like protein MED13L, a subunit of the CDK8-associated mediator complex that functions in transcriptional regulation through DNA-binding transcription factors and RNA polymerase II. Heterozygous MED13L variants cause transposition of the great arteries and intellectual disability (ID). Here, we report eight patients with predominantly novel MED13L variants who lack such complex congenital heart malformations. Rather, they depict a syndromic form of ID characterized by facial dysmorphism, ID, speech impairment, motor developmental delay with muscular hypotonia and behavioral difficu…

MaleAdolescentHeart malformationTransposition of Great VesselsRNA polymerase IIBioinformaticsArticleMediatorIntellectual DisabilityIntellectual disabilityGeneticsmedicineTranscriptional regulationHumansAbnormalities MultipleChildTranscription factorGenetics (clinical)GeneticsScience & TechnologyMediator ComplexbiologyMuscular hypotoniaSyndromemedicine.diseasePhenotypeChild PreschoolMutationbiology.proteinMuscle HypotoniaFemaleNeurocognitiveEuropean Journal of Human Genetics
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Transcription intermediary factor 1γ is a tumor suppressor in mouse and human chronic myelomonocytic leukemia.

2011

Transcription intermediary factor 1γ (TIF1γ) was suggested to play a role in erythropoiesis. However, how TIF1γ regulates the development of different blood cell lineages and whether TIF1γ is involved in human hematological malignancies remain to be determined. Here we have shown that TIF1γ was a tumor suppressor in mouse and human chronic myelomonocytic leukemia (CMML). Loss of Tif1g in mouse HSCs favored the expansion of the granulo-monocytic progenitor compartment. Furthermore, Tif1g deletion induced the age-dependent appearance of a cell-autonomous myeloproliferative disorder in mice that recapitulated essential characteristics of human CMML. TIF1γ was almost undetectable in leukemic ce…

MaleAgingAntimetabolites AntineoplasticTumor suppressor geneCellular differentiationMolecular Sequence DataChronic myelomonocytic leukemiaReceptor Macrophage Colony-Stimulating FactorBiologyDecitabinechemistry.chemical_compoundMicemedicineAnimalsHumansGenes Tumor SuppressorPromoter Regions GeneticTranscription factorAgedAged 80 and overMice KnockoutBase SequenceGene Expression Regulation LeukemicCell DifferentiationLeukemia Myelomonocytic ChronicGeneral MedicineDNA MethylationMiddle Agedmedicine.diseaseTRIM33Hematopoietic Stem CellsMolecular biologyDemethylating agentHematopoiesisNeoplasm ProteinsSpecific Pathogen-Free OrganismsHaematopoiesischemistryDNA methylationCancer researchAzacitidineFemaleTranscription FactorsResearch ArticleThe Journal of clinical investigation
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Post-transcriptional analysis of rat mitochondrial D-3-hydroxybutyrate dehydrogenase control through development and physiological stages.

1991

Abstract The nuclear encoded mitochondrial D -3-hydroxybutyrate dehydrogenase (BDH) is synthesized in the cytosal as a larger precursor. This membrane enzyme which requires lecithin for activity plays an essential role in energy metabolism as a ketone bodies-converting enzyme. A cDNA clone of the rat liver enzyme encompassing an antigenic determinant peptide has been isolated after immunoscreening of a λ gt11 expression library. The nucleotide sequence of this 279-base cDNA insert contains a single open reading frame of 93 amino-acids, which represents about a third of the mature enzyme. Amino-acid sequence analysis predicts a hydrophobic stretch of 29 amino-acids long which probably functi…

MaleAgingBlotting WesternMolecular Sequence DataBiologyGene Expression Regulation EnzymologicEnzyme activatorHydroxybutyrate DehydrogenaseComplementary DNAImmunoscreeningGene expressionAnimalsAmino Acid SequenceCloning MolecularRNA Processing Post-TranscriptionalGenechemistry.chemical_classificationMessenger RNASex CharacteristicsBase SequenceEstradiolRats Inbred StrainsCell BiologyGeneral MedicineDNABlotting NorthernEmbryo MammalianMolecular biologyDietary FatsMitochondriaRatsOpen reading frameEnzymeBiochemistrychemistryOrgan SpecificityFemaleCorticosteroneBiology of the cell
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Differential expression of PGC-1α and metabolic sensors suggest age-dependent induction of mitochondrial biogenesis in Friedreich ataxia fibroblasts.

2011

11 pages, 6 figures. PMID:21687738[PubMed] PMCID: PMC3110204

MaleAgingMitochondrial DiseasesMitochondrial MyopathyUbiquinoneCardiomyopathylcsh:MedicineMitochondrionAMP-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesAntioxidantsAdenosine TriphosphateAMP-activated protein kinaseTrinucleotide RepeatsFibrosisMolecular Cell BiologyChildlcsh:ScienceHeat-Shock ProteinsRegulation of gene expressionMultidisciplinaryMovement DisordersbiologyNeuromuscular DiseasesMiddle AgedCatalasePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaCell biologyMitochondriaDNA-Binding ProteinsNeurologyDisease ProgressionMedicineFemalemedicine.symptomSignal TransductionResearch ArticleAdultcongenital hereditary and neonatal diseases and abnormalitiesAtaxiaAdolescentMitochondrial ProteinsmedicineGeneticsHumansBiologyAllelesGlutathione PeroxidaseSuperoxide Dismutaselcsh:RHuman GeneticsFibroblastsmedicine.diseaseMolecular biologyOxidative StressMitochondrial biogenesisGene Expression RegulationFriedreich Ataxiabiology.proteinFrataxinlcsh:QEnergy MetabolismReactive Oxygen SpeciesTranscription FactorsPLoS ONE
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