Search results for "Transferase"

showing 10 items of 1030 documents

Somatic copy number alterations are associated with EGFR amplification and shortened survival in patients with primary glioblastoma.

2019

Glioblastoma (GBM) is the most common malignant primary tumor of the central nervous system. With no effective therapy, the prognosis for patients is terrible poor. It is highly heterogeneous and EGFR amplification is its most frequent molecular alteration. In this light, we aimed to examine the genetic heterogeneity of GBM and to correlate it with the clinical characteristics of the patients. For that purpose, we analyzed the status of EGFR and the somatic copy number alterations (CNAs) of a set of tumor suppressor genes and oncogenes. Thus, we found GBMs with high level of EGFR amplification, low level and with no EGFR amplification. Highly amplified tumors showed histological features of…

0301 basic medicineMaleCancer ResearchBiopsyL-amp GB EGFR-low amplified glioblastomamedicine.disease_causewt wildtypeMYBPC3 myosin-binding protein C0302 clinical medicineHIC1 hypermethylated in cancer 1Gene duplicationIn Situ Hybridization FluorescenceIDH2 isocitrate dehydrogenase 2MutationRB-pat RB signaling pathwayEGFRvIII epidermal growth factor receptor variant number IIIPAH phenylalanine hydroxylaseGBM glioblastoma IDH-wildtype (glioblastoma multiforme primary glioblastoma).ANOVA ANalysis Of VArianceN-amp GB EGFR-no amplified glioblastomaMiddle AgedCDKN2A cyclin-dependent kinase inhibitor 2Alcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisPrimary tumorImmunohistochemistryH-amp GB EGFR-high amplified glioblastomaErbB ReceptorsTKR-pat tyrosine-kinase receptors signaling pathway030220 oncology & carcinogenesisDisease ProgressionCDK6 cyclin-dependent kinase 6CDH1 Cadherin 1FemaleCREM cAMP response element modulatorIHC immunohistochemistryAdultOriginal articleDNA Copy Number VariationsCDKN1B cyclin-dependent kinase inhibitor 1BBiologyRARB retinoic acid receptor betaCNS central nervous systemlcsh:RC254-282IDH1 isocitrate dehydrogenase 1BCL2 B-cell cll/ lymphoma 2CNAs copy number algerationsWHO World Health Organization03 medical and health sciencesYoung Adultp53-pat p53 signaling pathwaymedicineBiomarkers TumorTMA tissue microarrayPTENHumansProtein kinase BPI3K/AKT/mTOR pathwaySurvival analysisAgedGenetic heterogeneityGene AmplificationGFAP glial fibrillary acidic proteinMLPA multiplex ligation-dependent probe amplificationmedicine.diseaseFISH fluorescence in situ hibridizationSurvival AnalysisCDKN2B cyclin-dependent kinase inhibitor 2BPTEN phosphatase and tensin homologEGFR epidermal growth factor receptorCNV-load load of copy number variations030104 developmental biologyMutationPARK2 parkinCancer researchbiology.proteinTCGA The Cancer Genome AtlasLARGE1 acetylglucosaminyltransferase-like protein 1GlioblastomaCHD7 Chromodomain Helicase DNA Binding Protein 7DAPI 4′6-diamidino-2-phenylindoleNeoplasia (New York, N.Y.)
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Novel multiple sclerosis susceptibility loci implicated in epigenetic regulation

2016

Genome-wide study in Germans identifies four novel multiple sclerosis risk genes and confirms already known gene loci.

0301 basic medicineMaleDLEU1MedizinGenome-wide association studyEpigenesis GeneticCohort StudiesResearch ArticlesTranscriptional Regulator ERGGeneticsAged 80 and overGlycine Hydroxymethyltransferaseeducation.field_of_studyMultidisciplinaryDNA methylationSciAdv r-articlesMiddle AgedSHMT13. Good healthddc:DNA-Binding ProteinsERGDNA methylationFemaleMAZFunction and Dysfunction of the Nervous SystemResearch ArticleAdultAdolescentPopulationQuantitative Trait Loci610 Medicine & healthDleu1 ; Dna Methylation ; Erg ; L3mbtl3 ; Maz ; Multiple Sclerosis ; Shmt1 ; Genome-wide Association StudyQuantitative trait locusBiologyMajor histocompatibility complexNeurological DisordersMultiple sclerosis03 medical and health sciencesYoung AdultTranscriptional Regulator ERGHumansGenetic Predisposition to DiseaseL3MBTL3EpigeneticsAlleleeducationAllelesAgedgenome-wide association study030104 developmental biologyGenetic LociCase-Control Studiesbiology.proteinTranscription Factors
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Broad neurodevelopmental features and cortical anomalies associated with a novel de novo KMT2A variant in Wiedemann-Steiner syndrome.

2021

Abstract Wiedemann-Steiner syndrome (WDSTS) is a rare genetic disorder including developmental delay/intellectual disability (DD/ID), hypertrichosis cubiti, short stature, and distinctive facial features, caused by mutation in KMT2A gene, which encodes a histone methyltransferase (H3K4) that regulates chromatin-mediated transcription. Different neurodevelopmental phenotypes have been described within the WDSTS spectrum, including a peculiar Autism Spectrum Disorder (ASDs) subtype in some affected individuals. Here, we report a 9-year-old Caucasian male found by next-generation panel sequencing to carry a novel heterozygous de novo KMT2A frameshift variant (NM_001197104.2:c.4433delG; p. Arg1…

0301 basic medicineMaleDevelopmental Disabilities030105 genetics & heredityBiologyFocal cortical dysplasiaPalilaliaFrameshift mutation03 medical and health sciencesHypertrichosis cubitiIntellectual DisabilityGeneticsmedicineHumansChildFrameshift MutationGenetics (clinical)GeneticsCerebral CortexWiedemann-steiner syndrome.Genetic disorderHypertrichosis cubitiGeneral MedicineHistone-Lysine N-MethyltransferaseSyndromeKMT2ACortical dysplasiamedicine.diseasePalilaliaMalformations of Cortical Development030104 developmental biologyKMT2AWiedemann-Steiner syndromeAutism spectrum disorderbiology.proteinmedicine.symptomMyeloid-Lymphoid Leukemia ProteinEuropean journal of medical genetics
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Blimp1 Prevents Methylation of Foxp3 and Loss of Regulatory T Cell Identity at Sites of Inflammation

2018

Summary Foxp3+ regulatory T (Treg) cells restrict immune pathology in inflamed tissues; however, an inflammatory environment presents a threat to Treg cell identity and function. Here, we establish a transcriptional signature of central nervous system (CNS) Treg cells that accumulate during experimental autoimmune encephalitis (EAE) and identify a pathway that maintains Treg cell function and identity during severe inflammation. This pathway is dependent on the transcriptional regulator Blimp1, which prevents downregulation of Foxp3 expression and “toxic” gain-of-function of Treg cells in the inflamed CNS. Blimp1 negatively regulates IL-6- and STAT3-dependent Dnmt3a expression and function …

0301 basic medicineMaleEncephalomyelitis Autoimmune ExperimentalBlimp1CNS2Regulatory T cellInflammationchemical and pharmacologic phenomenaBiologyT-Lymphocytes RegulatoryGeneral Biochemistry Genetics and Molecular BiologyArticleepigenetic regulationDNA Methyltransferase 3AEpigenesis Genetic03 medical and health sciencesGenomic ImprintingMice0302 clinical medicineImmune systemDownregulation and upregulationmedicineAnimalsEpigeneticsDNA (Cytosine-5-)-Methyltransferaseslcsh:QH301-705.5Regulation of gene expressionInterleukin-6FOXP3Forkhead Transcription FactorsDNA methyltransferaseshemic and immune systemsDNA Methylation3. Good healthCell biologyddc:Mice Inbred C57BL030104 developmental biologymedicine.anatomical_structureregulatory T cellslcsh:Biology (General)inflammationFoxp3DNA methylationFemalePositive Regulatory Domain I-Binding Factor 1medicine.symptomCNS030217 neurology & neurosurgeryCell Reports
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Expanding the Phenotype Associated with NAA10-Related N-Terminal Acetylation Deficiency

2016

International audience; N-terminal acetylation is a common protein modification in eukaryotes associated with numerous cellular processes. Inherited mutations in NAA10, encoding the catalytic subunit of the major N-terminal acetylation complex NatA have been associated with diverse, syndromic X-linked recessive disorders, whereas de novo missense mutations have been reported in one male and one female individual with severe intellectual disability but otherwise unspecific phenotypes. Thus, the full genetic and clinical spectrum of NAA10 deficiency is yet to be delineated. We identified three different novel and one known missense mutation in NAA10, de novo in 11 females, and due to maternal…

0301 basic medicineMaleModels MolecularMicrocephalyMutation MissenseBiologyGermlineKEY WORDS: NAA1003 medical and health sciencesGermline mutationGenes X-LinkedIntellectual disabilityGeneticsmedicineMissense mutationHumansGenetic Predisposition to DiseaseN-Terminal Acetyltransferase EGenetics (clinical)Genetic Association StudiesGerm-Line MutationN-Terminal Acetyltransferase AResearch ArticlesGeneticsX-linked[SDV.GEN]Life Sciences [q-bio]/GeneticsRegional Council of BurgundyMosaicismN-terminal acetylationAcetylationmedicine.diseasePhenotypePedigreeOgden SyndromeX‐linked030104 developmental biologyNAA10intellectual disabilityN‐terminal acetylationContract grant sponsors: Dijon University HospitalFemale[ SDV.GEN ] Life Sciences [q-bio]/GeneticsNAA15Research ArticleHuman Mutation
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Combined effects of the PNPLA3 rs738409, TM6SF2 rs58542926, and MBOAT7 rs641738 variants on NAFLD severity: a multicenter biopsy-based study.

2016

The PNPLA3 p.I148M, TM6SF2 p.E167K, and MBOAT7 rs641738 variants represent genetic risk factors for nonalcoholic fatty liver disease (NAFLD). Here we investigate if these polymorphisms modulate both steatosis and fibrosis in patients with NAFLD. We recruited 515 patients with NAFLD (age 16–88 years, 280 female patients). Liver biopsies were performed in 320 patients. PCR-based assays were used to genotype the PNPLA3, TM6SF2, and MBOAT7 variants. Carriers of the PNPLA3 and TM6SF2 risk alleles showed increased serum aspartate aminotransferase and alanine transaminase activities (P 0.05). The MBOAT7 variant was solely associated with increased fibrosis (P = 0.046). In the multivariate model, v…

0301 basic medicineMalePathologyBiopsyBiochemistryGastroenterologySeverity of Illness Index0302 clinical medicineEndocrinologyFibrosisNon-alcoholic Fatty Liver DiseaseGenotypeNonalcoholic fatty liver diseaseAged 80 and overeducation.field_of_studybiologyFatty liverMiddle AgedLiver030211 gastroenterology & hepatologyFemaleAdultmedicine.medical_specialtyAdolescentGenotypePolymorphism Single Nucleotide03 medical and health sciencesYoung AdultInternal medicinemedicineHumansAdiponutrinGenetic Predisposition to DiseaseeducationAllelesGenetic Association StudiesAgedbusiness.industryMembrane ProteinsCell BiologyLipasemedicine.diseaseFibrosisFatty Liver030104 developmental biologyAlanine transaminasebiology.proteinSteatosisbusinessPatient-Oriented and Epidemiological ResearchAcyltransferasesTM6SF2Journal of lipid research
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Circadian and Dopaminergic Regulation of Fatty Acid Oxidation Pathway Genes in Retina and Photoreceptor Cells.

2016

The energy metabolism of the retina might comply with daily changes in energy demand and is impaired in diabetic retinopathy-one of the most common causes of blindness in Europe and the USA. The aim of this study was to investigate putative adaptation of energy metabolism in healthy and diabetic retina. Hence expression analysis of metabolic pathway genes was performed using quantitative polymerase chain reaction, semi-quantitative western blot and immunohistochemistry. Transcriptional profiling of key enzymes of energy metabolism identified transcripts of mitochondrial fatty acid β-oxidation enzymes, i.e. carnitine palmitoyltransferase-1α (Cpt-1α) and medium chain acyl-CoA dehydrogenase (A…

0301 basic medicineMalePhysiologyDopamineMice ObeseGene Expressionlcsh:MedicineBiochemistryAcyl-CoA DehydrogenaseMice0302 clinical medicineCatecholaminesEndocrinologyMedicine and Health SciencesAminesEnzyme Chemistrylcsh:ScienceBeta oxidationMice KnockoutMice Inbred C3HMultidisciplinaryOrganic CompoundsDopaminergicFatty AcidsNeurochemistryDiabetic retinopathyNeurotransmittersCircadian RhythmChemistryCircadian Oscillatorsmedicine.anatomical_structurePhysical SciencesFemaleAnatomyOxidation-Reductionmedicine.drugResearch Articlemedicine.medical_specialtyBiogenic AminesEndocrine DisordersOcular AnatomyBiologyRetinaEnzyme Regulation03 medical and health sciencesOcular SystemInternal medicinemedicineGeneticsDiabetes MellitusAnimalsPhotoreceptor CellsGene RegulationCircadian rhythmCarnitineACADMRetinaDiabetic RetinopathyCarnitine O-PalmitoyltransferaseReceptor Melatonin MT1Receptors Dopamine D4Organic Chemistrylcsh:RChemical CompoundsBiology and Life Sciencesmedicine.diseaseHormonesMice Inbred C57BLMetabolic pathwayDisease Models Animal030104 developmental biologyEndocrinologyMetabolismMicroscopy FluorescenceMetabolic DisordersEnzymologylcsh:Qsense organsEnergy MetabolismPhysiological ProcessesChronobiology030217 neurology & neurosurgeryNeurosciencePLoS ONE
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Mitochondrial Fatty Acid β-Oxidation Inhibition Promotes Glucose Utilization and Protein Deposition through Energy Homeostasis Remodeling in Fish.

2020

BACKGROUND: Fish cannot use carbohydrate efficiently and instead utilize protein for energy supply, thus limiting dietary protein storage. Protein deposition is dependent on protein turnover balance, which correlates tightly with cellular energy homeostasis. Mitochondrial fatty acid β-oxidation (FAO) plays a crucial role in energy metabolism. However, the effect of remodeled energy homeostasis caused by inhibited mitochondrial FAO on protein deposition in fish has not been intensively studied. OBJECTIVES: This study aimed to identify the regulatory role of mitochondrial FAO in energy homeostasis maintenance and protein deposition by studying lipid, glucose, and protein metabolism in fish. M…

0301 basic medicineMaleProtein metabolismMedicine (miscellaneous)MitochondrionEnergy homeostasis03 medical and health scienceschemistry.chemical_compoundNile tilapia0302 clinical medicineAdjuvants ImmunologicmedicineAnimalsHomeostasisInsulinCarnitineProtein kinase ACells CulturedZebrafishNutrition and DieteticsbiologyCarnitine O-PalmitoyltransferaseChemistryFatty AcidsProtein turnoverProteinsMetabolismCichlidsDNACytochromes bbiology.organism_classificationMitochondria030104 developmental biologyGlucoseBiochemistryMutationHepatocytesNutrient Physiology Metabolism and Nutrient-Nutrient InteractionsEnergy MetabolismOxidation-Reduction030217 neurology & neurosurgerymedicine.drugMethylhydrazinesThe Journal of nutrition
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Homocysteine concentration in coronary artery disease: Influence of three common single nucleotide polymorphisms.

2017

Whether single nucleotide polymorphisms (SNPs) of homocysteine metabolism enzymes influence the rate of cardiovascular (CV) events in coronary artery disease (CAD) patients remains controversial.In this analysis, 1126 subjects from the AtheroGene study with CAD and 332 control subjects without known CAD were included. The following SNPs were investigated: methylentetrahydrofolate reductase (MTHFR-C667T), methionin synthetase (MS-D919G), and cystathionin beta synthetase (CBS-I278T). The endpoint was the combination of cardiovascular death, stroke, and non-fatal myocardial infarction (N = 286). The median follow-up time was 6.4 years. Kaplan-Meier curve analysis showed an increasing event rat…

0301 basic medicineMaleTime FactorsHomocysteineEndocrinology Diabetes and MetabolismMyocardial InfarctionMedicine (miscellaneous)Coronary Artery DiseaseKaplan-Meier Estimate030204 cardiovascular system & hematologyReductaseGastroenterology5-Methyltetrahydrofolate-Homocysteine S-MethyltransferaseCoronary artery diseasechemistry.chemical_compound0302 clinical medicineGene FrequencyRisk FactorsMyocardial infarctionStrokeHomocysteineGeneticsNutrition and DieteticsbiologyHomozygoteMiddle AgedStrokePhenotypeArea Under CurveDisease ProgressionFemaleCardiology and Cardiovascular Medicinemedicine.medical_specialtyHeterozygoteCystathionine beta-SynthaseSingle-nucleotide polymorphismPolymorphism Single NucleotideRisk Assessment03 medical and health sciencesPredictive Value of TestsInternal medicinemedicineHumansGenetic Predisposition to DiseaseGenetic Association StudiesMethylenetetrahydrofolate Reductase (NADPH2)AgedProportional Hazards ModelsChi-Square DistributionCurve analysismedicine.disease030104 developmental biologychemistryROC CurveMethylenetetrahydrofolate reductaseCase-Control Studiesbiology.proteinBiomarkersNutrition, metabolism, and cardiovascular diseases : NMCD
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Sequential cleavage of the proteins encoded by HNOT/ALG3, the human counterpart of the Drosophila NOT and yeast ALG3 gene, results in products acting…

2017

This study provides first insights into the biosynthesis, structure, biochemistry and complex processing of the proteins encoded by hNOT/ALG3, the human counterpart of the Drosophila Neighbour of TID (NOT) and the yeast asparagine linked glycosylation 3 gene (ALG3), which encodes a mannosyltransferase. Unambiguous evidence that both the fly and human proteins act as mannosyltransferases has not been provided yet. Previously, we showed that hNOT/ALG3 encodes two alternatively spliced main transcripts, hNOT-1/ALG3-1 and hNOT-4/ALG3-4, and their 15 truncated derivatives that lack diverse sets of exons and/or carry point mutations that result in premature termination codons. Here we show that t…

0301 basic medicineMannosyltransferaseGlycosylationSaccharomyces cerevisiae ProteinsGlycosylationProtein ConformationRNA SplicingSaccharomyces cerevisiaeBiologyMannosyltransferases03 medical and health scienceschemistry.chemical_compoundExonNuclear Receptor Subfamily 4 Group A Member 2GeneticsAnimalsHumansAmino Acid SequenceAsparagineMolecular BiologyGeneGenetics (clinical)Cellular compartmentPoint mutationComputational BiologyMembrane ProteinsExonsGeneral MedicineCell biologyAlternative Splicing030104 developmental biologychemistryCodon NonsenseDrosophilaCytokinesisHuman Molecular Genetics
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