Hypoxia-inducible factor-1 is a major transcription factor composed of two subunits: HIF-1alpha and HIF-1 beta. Under normoxic conditions, HIF-1 alpha is targeted to proteosomal degradation via ubiquitination. On the other hand during hypoxic conditions when oxygen concentration is low, HIF-1 alpha is stabilized and translocates to nucleus, where it dimerises with HIF-1 beta to form functional HIF-1. This altered redox state occurring in the cells experiencing hypoxia in turn indicates gene transcription of several angiogenic factors.
-Western%20Blot-NB100-105-img0005.jpg "Western Blot: HIF-1 alpha Antibody")
HIF-1 is a key transcription factor that regulates blood vessel formation by affecting the expression of vascular endothelial growth factor (VEGF). It has a key role in cellular responses to hypoxia in both normal and malignant cells. As HIF-1 alpha is a heterodimeric transcription factor composed of oxygen-dependent HIF-1 alpha and constitutively expressed HIF-1 beta subunits, HIF-1 transcriptional activity is largely determined by regulated expression of the HIF-1 alpha subunit (1). Although HIF-1 alpha is stabilized under hypoxic conditions because of its oxygen-dependent degradation domain that binds with the von-Hippel-Lindau protein (VHL)-containing complex, non-hypoxic activation of HIF-1 alpha by cytokines, oncogenes, and reactive oxygen species has also been reported (2). Nuclear expressions of HIF-1 alpha and other transcription factors were assessed in 251 human gastric carcinoma specimens by immunohistochemical tissue array analysis which demonstrated increased expression of HIF-1 alpha (3). Although hypoxia is the main stimulator of HIFs activity, also in normoxic conditions numerous stimuli like reactive oxygen species, metal ions or growth factors may lead to the enhancement of HIFs levels.
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