Search results for "Epigenetic"

showing 10 items of 632 documents

Paternal uniparental disomy chromosome 14-like syndrome due a maternal de novo 160 kb deletion at the 14q32.2 region not encompassing the IG- and the…

2015

The human chromosome 14q32 carries a cluster of imprinted genes which include the paternally expressed genes (PEGs) DLK1 and RTL1, as well as the maternally expressed genes (MEGs) MEG3, RTL1as, and MEG8. PEGs and MEGs expression at the 14q32.2-imprinted region are regulated by two differentially methylated regions (DMRs): the IG-DMR and the MEG3-DMR, which are respectively methylated on the paternal and unmethylated on the maternal chromosome 14 in most cells. Genetic and epigenetic abnormalities affecting these imprinted gene clusters result in two different phenotypes currently known as maternal upd(14) syndrome and paternal upd(14) syndrome. However, only few patients carrying a maternal…

14q32.2 imprinted regionGenotypeBiologyPregnancy ProteinsMEG3-DMRGenomic ImprintingPaternal uniparental disomy chromosome 14 [upd(14)pat]GeneticsmedicineHumans14q32.2 maternal deletionEpigenetics"coat-hanger" rib signGeneGenetics (clinical)Sequence DeletionGeneticsMEG3Chromosomes Human Pair 14Comparative Genomic HybridizationIG-DMRMEG3 geneCalcium-Binding ProteinsInfant NewbornChromosomeMembrane ProteinsSyndromeDNA MethylationUniparental Disomymedicine.diseasePrognosisPhenotypeMolecular biologyUniparental disomyDifferentially methylated regionsPhenotypeSkeletal dysplasiaIntercellular Signaling Peptides and ProteinsFemaleRNA Long NoncodingRTL1as geneGenomic imprintingAmerican journal of medical genetics. Part A
researchProduct

Genetic and Epigenetic Factors of Takotsubo Syndrome: A Systematic Review

2021

Takotsubo syndrome (TTS), recognized as stress’s cardiomyopathy, or as left ventricular apical balloon syndrome in recent years, is a rare pathology, described for the first time by Japanese researchers in 1990. TTS is characterized by an interindividual heterogeneity in onset and progression, and by strong predominance in postmenopausal women. The clear causes of these TTS features are uncertain, given the limited understanding of this intriguing syndrome until now. However, the increasing frequency of TTS cases in recent years, and particularly correlated to the SARS-CoV-2 pandemic, leads us to the imperative necessity both of a complete knowledge of TTS pathophysiology for identifying bi…

2019-20 coronavirus outbreakTTS managementCoronavirus disease 2019 (COVID-19)DNA Copy Number VariationsQH301-705.5Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)Heart VentriclesReviewBioinformaticsPolymorphism Single NucleotideCatalysisEpigenesis GeneticInorganic ChemistryGenetic Heterogeneitysystematic reviewTakotsubo CardiomyopathyMedicineHumansGenetic Predisposition to DiseaseEpigeneticsTakotsubo cardiomyopathy (TTS)Biology (General)Physical and Theoretical ChemistryMedical History TakingQD1-999Molecular BiologySpectroscopyTakotsubo syndromePostmenopausal womenbusiness.industryGenetic heterogeneitySARS-CoV-2Organic ChemistrybiomarkersCOVID-19General Medicinespecific and effective treatmentsgenetic and epigenetic factorsComputer Science ApplicationsChemistrySettore MED/03Genetic LociIdentification (biology)businessInternational Journal of Molecular Sciences
researchProduct

The influence of serotonin- and other genes on impulsive behavioral aggression and cognitive impulsivity in children with attention-deficit/hyperacti…

2008

Contains fulltext : 70708.pdf (Publisher’s version ) (Open Access) ABSTRACT: BACKGROUND: Low serotonergic (5-HT) activity correlates with increased impulsive-aggressive behavior, while the opposite association may apply to cognitive impulsiveness. Both types of impulsivity are associated with attention-deficit/hyperactivity disorder (ADHD), and genes of functional significance for the 5-HT system are implicated in this disorder. Here we demonstrate the separation of aggressive and cognitive components of impulsivity from symptom ratings and test their association with 5-HT and functionally related genes using a family-based association test (FBAT-PC). METHODS: Our sample consisted of 1180 o…

2805 Cognitive Neurosciencemedicine.medical_specialtyNeurologyGenetics and epigenetic pathways of disease [NCMLS 6]Cognitive NeuroscienceMedizin610 Medicine & healthNeuroinformatics [DCN 3]SerotonergicImpulsivityMental health [NCEBP 9]lcsh:RC346-429Genomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesBehavioral Neuroscience0302 clinical medicineCognitive neurosciences [UMCN 3.2]2802 Behavioral NeurosciencePerception and Action [DCN 1]medicineAttention deficit hyperactivity disorderddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und JugendaltersAssociation (psychology)Psychiatrylcsh:Neurology. Diseases of the nervous systemBiological PsychiatryAggressionResearchCognitionGeneral Medicine10058 Department of Child and Adolescent Psychiatrymedicine.disease030227 psychiatryAutism spectrum disordermedicine.symptomPsychologyFunctional Neurogenomics [DCN 2]2803 Biological Psychiatry030217 neurology & neurosurgeryClinical psychology
researchProduct

Direct Reprogramming of Somatic Cells into Induced Neuronal Cells: Where We Are and Where We Want to Go

2014

Direct reprogramming of somatic cells has emerged as a novel strategy to generate neurons, including those of human origin. The method provides enormous potential for studying the mechanisms directing neuronal differentiation, the modeling of neurodegenerative diseases, and the development of potential novel approaches for brain repair. In this chapter, we briefly trace the history of reprogramming, as well as the strategies employed to date for converting different types of somatic cells, including fibroblasts, hepatocytes, astrocytes, and pericytes into induced neuronal cells of different subtype identity. Reprogramming involves particular emphasis on transcriptional and posttranscription…

ASCL1Somatic cellRegeneration (biology)NeurogenesismicroRNAEpigeneticsBiologyTranscription factorNeuroscienceReprogramming
researchProduct

Cytotoxicity of 35 medicinal plants from Sudan towards sensitive and multidrug-resistant cancer cells

2015

Abstract Background Cancer is a complex disease with multiple genetic and epigenetic alterations. Since decades, the hallmark of cancer therapy is chemotherapy. Cytotoxic drugs erase rapidly dividing cells without sufficient differentiation between normal and cancerous cells resulting in severe side effects in normal tissues. Recently, strategies for cancer treatment focused on targeting specific proteins involved in tumor growth and progression. The present study was designed to investigate the cytotoxicity of 65 crude extracts from 35 Sudanese medicinal plants towards various cancer cell lines expressing molecular mechanisms of resistance towards classical chemotherapeutics (two ATP-bindi…

ATP Binding Cassette Transporter Subfamily BCytoskeleton organizationCell SurvivalDNA repairBiologyPharmacologySudanSesquiterpenes GuaianeImmune systemCell Line TumorOxazinesDrug DiscoveryHumansATP Binding Cassette Transporter Subfamily B Member 1EpigeneticsCytotoxicityPharmacologyPlants MedicinalComputational BiologyAntineoplastic Agents PhytogenicDrug Resistance MultipleGene expression profilingXanthenesDrug Resistance NeoplasmPharmacogeneticsCell cultureCancer cellCancer researchIndicators and ReagentsTumor Suppressor Protein p53SesquiterpenesJournal of Ethnopharmacology
researchProduct

CNGB3 mutations account for 50% of all cases with autosomal recessive achromatopsia

2005

Contains fulltext : 47591.pdf (Publisher’s version ) (Closed access) Achromatopsia is a congenital, autosomal recessively inherited disorder characterized by a lack of color discrimination, low visual acuity (<0.2), photophobia, and nystagmus. Mutations in the genes for CNGA3, CNGB3, and GNAT2 have been associated with this disorder. Here, we analyzed the spectrum and prevalence of CNGB3 gene mutations in a cohort of 341 independent patients with achromatopsia. In 163 patients, CNGB3 mutations could be identified. A total of 105 achromats carried apparent homozygous mutations, 44 were compound (double) heterozygotes, and 14 patients had only a single mutant allele. The derived CNGB3 mutatio…

AchromatopsiaGenetics and epigenetic pathways of disease [NCMLS 6]genetic structuresGATED CATION CHANNELCNGB3 mutationsNonsense mutationMutantCyclic Nucleotide-Gated Cation ChannelsColor Vision DefectsGenes RecessiveLocus (genetics)Gene mutationBiologyTOTAL COLOURBLINDNESSIon ChannelsCLONINGDogscyclic nucleotide-gated channelGNAT2GeneticsmedicineLOCUSAnimalsHumansMissense mutationNeurosensory disorders [UMCN 3.3]ACHM3 locusDog DiseasesAlleleAllelesGenetics (clinical)Geneticstotal colorblindnessGNAT2PHOTORECEPTORSDYSTROPHYmedicine.diseaseCONE DEGENERATIONGENEeye diseasesPhenotypeEvaluation of complex medical interventions [NCEBP 2]MutationRetinal Cone Photoreceptor Cellssense organsachromatopsiarod monochromacyALPHA-SUBUNIThuman activities
researchProduct

Blastic plasmacytoid dendritic cell neoplasm: genomics mark epigenetic dysregulation as a primary therapeutic target

2018

Blastic Plasmacytoid Dendritic Cell Neoplasm is a rare and aggressive hematological malignancy currently lacking an effective therapy. To possibly identify genetic alterations useful for a new treatment design, we analyzed by whole-exome sequencing fourteen Blastic Plasmacytoid Dendritic Cell Neoplasm patients and the patient-derived CAL-1 cell line. The functional enrichment analysis of mutational data reported the epigenetic regulatory program as the most significantly undermined (P&lt;.0001). In particular, twenty-five epigenetic-modifiers were found mutated (e.g., ASXL1, TET2, SUZ12, ARID1A, PHF2, CHD8); ASXL1 was the most frequently affected (28.6% of cases). To evaluate the impact of …

Acute Myeloid LeukemiaBlastic plasmacytoid dendritic cell neoplasm epigenetic mutationsSkin NeoplasmsAzacitidineDecitabinePlasmacytoid dendritic cellGene mutationBiologyDecitabineBPDCNArticleEpigenesis Genetic03 medical and health sciences0302 clinical medicineHistone methylation5’-Azacytidine; Acute Myeloid Leukemia; BPDCN; Decitabine; WESmedicineHumansEpigeneticsExome sequencingRegulation of gene expressionMyeloproliferative DisordersDendritic CellsGenomicsHematology5 -AzacytidineMyeloid Neoplasms5’-AzacytidineCancer researchWES030215 immunologymedicine.drugHaematologica
researchProduct

TP53 and p16INK4A, but not H-KI-Ras, are involved in tumorigenesis and progression of pleomorphic adenomas.

2006

The putative role of TP53 and p16INK4A tumor suppressor genes and Ras oncogenes in the development and progression of salivary gland neoplasias was studied in 28 cases of pleomorphic adenomas (PA), 4 cases of cystic adenocarcinomas, and 1 case of carcinoma ex-PA. Genetic and epigenetic alterations in the above genes were analyzed by Polymerase Chain Reaction/Single Strand Conformational Polymorphism (PCR/SSCP) and sequencing and by Methylation Specific-PCR (MS-PCR). Mutations in TP53 were found in 14% (4/28) of PAs and in 60% (3/5) of carcinomas. Mutations in H-Ras and K-Ras were identified in4%(1/28) and7% (2/28) of PAs, respectively. Only 20% (1/5) of carcinomas screened displayed mutatio…

AdenomaAdenomaGenotypePhysiologyClinical BiochemistryBiologymedicine.disease_causeMethylationEpigenesis GeneticProto-Oncogene Proteins p21(ras)GenotypemedicineCarcinomaHumansEpigeneticsTP53GeneCyclin-Dependent Kinase Inhibitor p16Base SequenceSingle-strand conformation polymorphismCell BiologyMethylationmedicine.diseaseMolecular biologyCell Transformation NeoplasticMutationDisease ProgressionTumor Suppressor Protein p53Carcinogenesis
researchProduct

Customised next-generation sequencing multigene panel to screen a large cohort of individuals with chromatin-related disorder

2020

BackgroundThe regulation of the chromatin state by epigenetic mechanisms plays a central role in gene expression, cell function, and maintenance of cell identity. Hereditary disorders of chromatin regulation are a group of conditions caused by abnormalities of the various components of the epigenetic machinery, namely writers, erasers, readers, and chromatin remodelers. Although neurological dysfunction is almost ubiquitous in these disorders, the constellation of additional features characterizing many of these genes and the emerging clinical overlap among them indicate the existence of a community of syndromes. The introduction of high-throughput next generation sequencing (NGS) methods f…

Adenosine TriphosphataseAdultMaleCCCTC-Binding FactorTranscription FactorDNA-Binding Proteinchromatin disorderComputational biologyBiologyDNA HelicaseDNA sequencingEpigenesis GeneticMendelian chromatin disordersLocus heterogeneityDe Lange SyndromeGeneticsmedicineCoffin-Lowry SyndromeHumansGenetic Predisposition to DiseaseEpigeneticsGenetic TestingChildGeneGenetics (clinical)Adenosine Triphosphatasesnext generation sequencingepigeneticsGenetic heterogeneityDNA HelicasesMendelian chromatin disorderHistone-Lysine N-Methyltransferasemedicine.diseaseChromatinChromatinDNA-Binding ProteinsMendelian chromatin disorders; epigenetics; next generation sequencingCohortMutationRelated disorderFemaleMyeloid-Lymphoid Leukemia ProteinepigeneticTranscription FactorsHuman
researchProduct

m6A RNA methylation of major satellite repeat transcripts facilitates chromatin association and RNA:DNA hybrid formation in mouse heterochromatin

2021

Abstract Heterochromatin has essential functions in maintaining chromosome structure, in protecting genome integrity and in stabilizing gene expression programs. Heterochromatin is often nucleated by underlying DNA repeat sequences, such as major satellite repeats (MSR) and long interspersed nuclear elements (LINE). In order to establish heterochromatin, MSR and LINE elements need to be transcriptionally competent and generate non-coding repeat RNA that remain chromatin associated. We explored whether these heterochromatic RNA, similar to DNA and histones, may be methylated, particularly for 5-methylcytosine (5mC) or methyl-6-adenosine (m6A). Our analysis in mouse ES cells identifies only b…

AdenosineAcademicSubjects/SCI00010HeterochromatinRNA methylationMethylationMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineHeterochromatinGene expressionGeneticsAnimals030304 developmental biology0303 health sciencesbiologyMethyltransferase complexGene regulation Chromatin and EpigeneticsRNAMouse Embryonic Stem CellsDNAChromatinCell biologyHistonechemistryTandem Repeat Sequencesbiology.proteinRNA030217 neurology & neurosurgeryDNANucleic Acids Research
researchProduct