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dc.contributor.authorTarhriz, V
dc.contributor.authorWagner, KD
dc.contributor.authorMasoumi, Z
dc.contributor.authorMolavi, O
dc.contributor.authorHejazi, MS
dc.contributor.authorGhanbarian, H
dc.date.accessioned2018-08-26T04:59:06Z
dc.date.available2018-08-26T04:59:06Z
dc.date.issued2018
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/38814
dc.description.abstractCdk9 is the catalytic core of the positive transcription elongation factor b (P-TEFb) and regulates transcriptional elongation factors by phosphorylation of RNA pol II. Apart from its role on myogenic gene expression, Cdk9 regulation of muscle-specific microRNAs in the early stage of cardiomyogenesis is poorly understood. Here we demonstrate that Cdk9 not only regulates myogenic transcription factors, but also controls muscle-specific microRNAs. During cardiac differentiation of mouse embryonic stem cells, high Cdk9 expression preceded up-regulation of miR-1. To investigate potential regulatory roles of Cdk9 on cardiac microRNAs and myogenesis genes, we overexpressed Cdk9 in myoblast C2C12 cells, which resulted in significant induction of miR-1 and miR-206, while miR-133 was downregulated. Moreover, expression levels of MyoD and Srf, key regulators of myogenesis, also increased in cells with overexpression of Cdk9. We further observed Cdk9-mediated apoptosis in C2C12 cells corresponding to induction of miR-1 expression levels. Thus, Cdk9 plays a complex role in myocyte progenitor differentiation and apoptosis by regulating myogenic protein and muscle-specific microRNA expression. J. Cell. Biochem. 119: 547-554, 2018. é 2017 Wiley Periodicals, Inc.
dc.language.isoEnglish
dc.relation.ispartofJournal of cellular biochemistry
dc.subjectAnimals
dc.subjectApoptosis
dc.subjectCell Line
dc.subjectCyclin-Dependent Kinase 9
dc.subjectGene Expression Regulation
dc.subjectMice
dc.subjectMicroRNAs
dc.subjectMuscle Development
dc.subjectMyoblasts, Cardiac
dc.titleCDK9 Regulates Apoptosis of Myoblast Cells by Modulation of microRNA-1 Expression.
dc.typearticle
dc.citation.volume119
dc.citation.issue1
dc.citation.spage547
dc.citation.epage554
dc.citation.indexPubmed
dc.identifier.DOIhttps://doi.org/10.1002/jcb.26213


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