A network of regulations by small noncoding RNAs: the P TEFb kinase in development and pathology

Part of the heterodimeric PTEF-b element of the PolII transcription machinery, the Cdk9 kinase plays a critical role in gene expression. Phosphorylation of several residues in the polymerase is required for elongation of transcript. It determines the rates of transcription and thus, plays a critical...

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Main Authors: Hossein eGhanbarian, Valerie eGrandjean, Francois eCuzin, Minoo eRassoulzadegan
Format: Article
Language:English
Published: Frontiers Media S.A. 2011-12-01
Series:Frontiers in Genetics
Subjects:
Online Access:http://journal.frontiersin.org/Journal/10.3389/fgene.2011.00095/full
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author Hossein eGhanbarian
Hossein eGhanbarian
Valerie eGrandjean
Francois eCuzin
Minoo eRassoulzadegan
author_facet Hossein eGhanbarian
Hossein eGhanbarian
Valerie eGrandjean
Francois eCuzin
Minoo eRassoulzadegan
author_sort Hossein eGhanbarian
collection DOAJ
description Part of the heterodimeric PTEF-b element of the PolII transcription machinery, the Cdk9 kinase plays a critical role in gene expression. Phosphorylation of several residues in the polymerase is required for elongation of transcript. It determines the rates of transcription and thus, plays a critical role in several differentiation pathways, best documented in heart development. The synthesis and activity of the protein are tightly regulated in a coordinated manner by at least three noncoding RNAs. First, its kinase activity is reversibly inhibited by formation of a complex with the 334 nt 7SK RNA, from which it is released under conditions of stress. Then, heart development requires a maximal rate of synthesis during cardiomyocyte differentiation, followed by a decrease in the differentiated state. The latter is insured by microRNA-mediated translational inhibition. In a third mode of RNA control, increased levels of transcription are induced by small noncoding RNA molecules with sequences homologous to the transcript. Designated paramutation, this epigenetic variation, stable during development and hereditarily transmitted in a non-Mendelian manner over several generations, is thought to be a response to the inactivation of one of the two alleles by an abnormal recombination event such as insertion of a transposon.
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spelling doaj.art-d8f6342e1a04432f91ed1652af7a7a6e2022-12-21T19:44:08ZengFrontiers Media S.A.Frontiers in Genetics1664-80212011-12-01210.3389/fgene.2011.0009516813A network of regulations by small noncoding RNAs: the P TEFb kinase in development and pathologyHossein eGhanbarian0Hossein eGhanbarian1Valerie eGrandjean2Francois eCuzin3Minoo eRassoulzadegan4Institut National de la Santé et de la Recherche MédicaleStem Cell Technology Research CenterInstitut National de la Santé et de la Recherche MédicaleInstitut National de la Santé et de la Recherche MédicaleInstitut National de la Santé et de la Recherche MédicalePart of the heterodimeric PTEF-b element of the PolII transcription machinery, the Cdk9 kinase plays a critical role in gene expression. Phosphorylation of several residues in the polymerase is required for elongation of transcript. It determines the rates of transcription and thus, plays a critical role in several differentiation pathways, best documented in heart development. The synthesis and activity of the protein are tightly regulated in a coordinated manner by at least three noncoding RNAs. First, its kinase activity is reversibly inhibited by formation of a complex with the 334 nt 7SK RNA, from which it is released under conditions of stress. Then, heart development requires a maximal rate of synthesis during cardiomyocyte differentiation, followed by a decrease in the differentiated state. The latter is insured by microRNA-mediated translational inhibition. In a third mode of RNA control, increased levels of transcription are induced by small noncoding RNA molecules with sequences homologous to the transcript. Designated paramutation, this epigenetic variation, stable during development and hereditarily transmitted in a non-Mendelian manner over several generations, is thought to be a response to the inactivation of one of the two alleles by an abnormal recombination event such as insertion of a transposon.http://journal.frontiersin.org/Journal/10.3389/fgene.2011.00095/fullHeredityMiceepigeneticnoncoding RNAcardiac hypertrophy7sk
spellingShingle Hossein eGhanbarian
Hossein eGhanbarian
Valerie eGrandjean
Francois eCuzin
Minoo eRassoulzadegan
A network of regulations by small noncoding RNAs: the P TEFb kinase in development and pathology
Frontiers in Genetics
Heredity
Mice
epigenetic
noncoding RNA
cardiac hypertrophy
7sk
title A network of regulations by small noncoding RNAs: the P TEFb kinase in development and pathology
title_full A network of regulations by small noncoding RNAs: the P TEFb kinase in development and pathology
title_fullStr A network of regulations by small noncoding RNAs: the P TEFb kinase in development and pathology
title_full_unstemmed A network of regulations by small noncoding RNAs: the P TEFb kinase in development and pathology
title_short A network of regulations by small noncoding RNAs: the P TEFb kinase in development and pathology
title_sort network of regulations by small noncoding rnas the p tefb kinase in development and pathology
topic Heredity
Mice
epigenetic
noncoding RNA
cardiac hypertrophy
7sk
url http://journal.frontiersin.org/Journal/10.3389/fgene.2011.00095/full
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