Abstract
HIF-1 is the main transcription factor responsible for increased gene expression in hypoxia: VEGF, erythropoietin, GLUT-1, and glycolytic enzymes are such target genes and all participate in the adaptative response of cells to hypoxia. AP-1 activation by hypoxia has also been demonstrated in several cell lines and it cooperates with HIF-1 for increasing VEGF gene transcription in hypoxia. Both HIF-1 and AP-1 activation by hypoxia seems to involve members of the MAP kinase family. Here, we summarize the data indicating that ERK and JNK are needed for activation of HIF-1 and AP-1, respectively.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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DNA-Binding Proteins / metabolism*
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Endothelial Growth Factors / biosynthesis
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Endothelial Growth Factors / genetics
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Gene Expression Regulation*
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Humans
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Hypoxia / enzymology*
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Hypoxia / genetics*
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Hypoxia-Inducible Factor 1
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Hypoxia-Inducible Factor 1, alpha Subunit
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Lymphokines / biosynthesis
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Lymphokines / genetics
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Mitogen-Activated Protein Kinases / metabolism*
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Nuclear Proteins / metabolism*
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Transcription Factor AP-1 / metabolism*
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Transcription Factors*
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Vascular Endothelial Growth Factor A
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Vascular Endothelial Growth Factors
Substances
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DNA-Binding Proteins
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Endothelial Growth Factors
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HIF1A protein, human
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Hypoxia-Inducible Factor 1
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Hypoxia-Inducible Factor 1, alpha Subunit
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Lymphokines
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Nuclear Proteins
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Transcription Factor AP-1
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Transcription Factors
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Vascular Endothelial Growth Factor A
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Vascular Endothelial Growth Factors
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Mitogen-Activated Protein Kinases