Abstract
ChIP-chip and microarray expression studies show that, in response to hypoxia, HIF-1 preferentially binds to and up-regulates already active genes.
Highlights
Hypoxia-inducible factor 1 (HIF-1) plays a key role in cellular adaptation to hypoxia
Even after standardizing all of these variables, we verified by gene expression profiling that most hypoxia-induced changes in mRNA expression were cell type specific (Figure 1a)
Since a majority of HIF-1 binding sites in HepG2 cells were within promoter regions [2], we analyzed U87 HIF-1 chromatin immunoprecipitation (ChIP) samples on tiled arrays covering approximately 10 kb surrounding the transcriptional start sites (TSS) of all known genes
Summary
Hypoxia-inducible factor 1 (HIF-1) plays a key role in cellular adaptation to hypoxia. The transcription factor Hypoxia-inducible factor 1 (HIF-1) is a key mediator of cellular homeostasis in response to hypoxia. HIF-1 transactivates genes that facilitate metabolic adaptation by shifting from oxidative phosphorylation to anaerobic glycolysis, and enhances oxygen delivery by inducing vasodilatation, increasing vascular permeability, enhancing erythropoiesis, and angiogenesis [1]. Alignment of the sequences encompassing these HIF-1 binding sites has revealed a consensus core motif of 5'-A/ GCGTG-3'. It is clear that this promiscuous motif cannot be the sole determinant of HIF-1 binding and transactivation. As is the case for other transcription factors such as E2F1, Myc, estrogen receptor, FoxA1, and p63 [5,6,7,8], HIF-1 binds to only a small proportion of predicted binding sites
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
