Regulation of hypoxia-inducible gene expression after HIF activation

Norio Suzuki, Katarina Gradin, Lorenz Poellinger, Masayuki Yamamoto

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

Hypoxia causes dramatic changes in the expression profiles of genes that encode glycolytic enzymes, vascular endothelial growth factors, erythropoietin, and other factors in a tissue-specific manner through activating hypoxia-inducible transcription factors (HIFs) such as HIF1α and HIF2α. It has been elucidated that the activity of HIFs is fundamentally regulated by their protein stability in an oxygen-dependent manner. However, little is known about how stabilized HIFs regulate transcription of their target genes in hypoxic cells. Additionally, the roles of HIF3α, the third member of the HIFs, are still enigma due to its various splicing variants and the complicated phenotypes of Hif3a-gene modified mouse lines. Here, we summarize how molecular systems fine-tune hypoxia-inducible transcription with the cooperation of HIFs and their negative regulators, including IPAS, one of the HIF3α splicing variants. Since epigenetic mechanisms contribute to stress-inducible and cell-type specific gene regulation, the HIF-dependent reorganization of nucleosome structures in hypoxia-inducible gene promoters is also discussed.

Original languageEnglish
Pages (from-to)182-186
Number of pages5
JournalExperimental Cell Research
Volume356
Issue number2
DOIs
Publication statusPublished - 2017 Jul 15

Keywords

  • Chromatin
  • Epigenetics
  • Erythropoietin
  • Histone
  • Nucleosome
  • Transcription

ASJC Scopus subject areas

  • Cell Biology
  • Medicine(all)

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