Transcriptional regulation by hypoxia inducible factors

Abstract The cellular response to oxygen deprivation is governed largely by a family of transcription factors known as Hypoxia Inducible Factors (HIFs). This review focuses on the molecular mechanisms by which HIFs regulate the transcriptional apparatus to enable the cellular and organismal response...

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Published inCritical reviews in biochemistry and molecular biology Vol. 49; no. 1; pp. 1 - 15
Main Authors Dengler, Veronica L., Galbraith, Matthew D., Espinosa, Joaquín M.
Format Journal Article
LanguageEnglish
Published England Informa Healthcare USA, Inc 01.01.2014
Taylor & Francis
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Online AccessGet full text
ISSN1040-9238
1549-7798
1549-7798
DOI10.3109/10409238.2013.838205

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Abstract Abstract The cellular response to oxygen deprivation is governed largely by a family of transcription factors known as Hypoxia Inducible Factors (HIFs). This review focuses on the molecular mechanisms by which HIFs regulate the transcriptional apparatus to enable the cellular and organismal response to hypoxia. We discuss here how the various HIF polypeptides, their posttranslational modifications, binding partners and transcriptional cofactors affect RNA polymerase II activity to drive context-dependent transcriptional programs during hypoxia.
AbstractList The cellular response to oxygen deprivation is governed largely by a family of transcription factors known as Hypoxia Inducible Factors (HIFs). This review focuses on the molecular mechanisms by which HIFs regulate the transcriptional apparatus to enable the cellular and organismal response to hypoxia. We discuss here how the various HIF polypeptides, their post-translational modifications, binding partners and transcriptional cofactors affect RNA polymerase II activity to drive context-dependent transcriptional programs during hypoxia.
The cellular response to oxygen deprivation is governed largely by a family of transcription factors known as Hypoxia Inducible Factors (HIFs). This review focuses on the molecular mechanisms by which HIFs regulate the transcriptional apparatus to enable the cellular and organismal response to hypoxia. We discuss here how the various HIF polypeptides, their posttranslational modifications, binding partners and transcriptional cofactors affect RNA polymerase II activity to drive context-dependent transcriptional programs during hypoxia.
Abstract The cellular response to oxygen deprivation is governed largely by a family of transcription factors known as Hypoxia Inducible Factors (HIFs). This review focuses on the molecular mechanisms by which HIFs regulate the transcriptional apparatus to enable the cellular and organismal response to hypoxia. We discuss here how the various HIF polypeptides, their posttranslational modifications, binding partners and transcriptional cofactors affect RNA polymerase II activity to drive context-dependent transcriptional programs during hypoxia.
The cellular response to oxygen deprivation is governed largely by a family of transcription factors known as Hypoxia Inducible Factors (HIFs). This review focuses on the molecular mechanisms by which HIFs regulate the transcriptional apparatus to enable the cellular and organismal response to hypoxia. We discuss here how the various HIF polypeptides, their posttranslational modifications, binding partners and transcriptional cofactors affect RNA polymerase II activity to drive context-dependent transcriptional programs during hypoxia.The cellular response to oxygen deprivation is governed largely by a family of transcription factors known as Hypoxia Inducible Factors (HIFs). This review focuses on the molecular mechanisms by which HIFs regulate the transcriptional apparatus to enable the cellular and organismal response to hypoxia. We discuss here how the various HIF polypeptides, their posttranslational modifications, binding partners and transcriptional cofactors affect RNA polymerase II activity to drive context-dependent transcriptional programs during hypoxia.
Author Galbraith, Matthew D.
Dengler, Veronica L.
Espinosa, Joaquín M.
Author_xml – sequence: 1
  givenname: Veronica L.
  surname: Dengler
  fullname: Dengler, Veronica L.
  email: joaquin.espinosa@colorado.edu, joaquin.espinosa@colorado.edu
  organization: Howard Hughes Medical Institute & Department of Molecular, Cellular and Developmental Biology, The University of Colorado at Boulder, Boulder, CO, USA
– sequence: 2
  givenname: Matthew D.
  surname: Galbraith
  fullname: Galbraith, Matthew D.
  email: joaquin.espinosa@colorado.edu, joaquin.espinosa@colorado.edu
  organization: Howard Hughes Medical Institute & Department of Molecular, Cellular and Developmental Biology, The University of Colorado at Boulder, Boulder, CO, USA
– sequence: 3
  givenname: Joaquín M.
  surname: Espinosa
  fullname: Espinosa, Joaquín M.
  email: joaquin.espinosa@colorado.edu, joaquin.espinosa@colorado.edu
  organization: Howard Hughes Medical Institute & Department of Molecular, Cellular and Developmental Biology, The University of Colorado at Boulder, Boulder, CO, USA
BackLink https://www.ncbi.nlm.nih.gov/pubmed/24099156$$D View this record in MEDLINE/PubMed
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Snippet Abstract The cellular response to oxygen deprivation is governed largely by a family of transcription factors known as Hypoxia Inducible Factors (HIFs). This...
The cellular response to oxygen deprivation is governed largely by a family of transcription factors known as Hypoxia Inducible Factors (HIFs). This review...
SourceID pubmedcentral
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pubmed
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StartPage 1
SubjectTerms Animals
Chromatin
histones
Humans
hydroxylation
Hypoxia - genetics
Hypoxia - metabolism
hypoxia response element
Hypoxia-Inducible Factor 1 - chemistry
Hypoxia-Inducible Factor 1 - metabolism
mediator
p300
Protein Processing, Post-Translational
RNA polymerase II
RNA Polymerase II - metabolism
Transcriptional Activation
Title Transcriptional regulation by hypoxia inducible factors
URI https://www.tandfonline.com/doi/abs/10.3109/10409238.2013.838205
https://www.ncbi.nlm.nih.gov/pubmed/24099156
https://www.proquest.com/docview/1492674413
https://pubmed.ncbi.nlm.nih.gov/PMC4342852
Volume 49
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