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HIF1A — NOX4
Text-mined interactions from Literome
Haddad et al., Eur Cytokine Netw 2002
:
The
NADPH-oxidase inhibitor, 4'-hydroxy-3'-methoxy-acetophenone ( HMAP ), which may affect mitochondrial ROS production,
attenuated IL-1 beta mediated nuclear translocation and activation of
HIF-1 alpha
Yang et al., American journal of physiology. Renal physiology 2003
:
NAD ( P ) H oxidase activity may importantly
contribute to this posttranscriptional regulation of
HIF-1alpha in these cells under physiological conditions
Dong et al., Zhongguo Dang Dai Er Ke Za Zhi 2006
:
To study the
effect of
NADPH oxidase on hypoxia-inducible factor
(HIF)-1alpha and endothelin (ET)-1 expression in human umbilical endothelia cells ( HUVECs ) and its possible mechanism ... It is speculated that
NADPH oxidase as an oxygen sensor
regulates the
HIF-1alpha expression by changing the intracellular redox reaction and that except HIF-1, H2O2 might contribute to ET-1 synthesis and release
Oh et al., Neurosci Lett 2008
(Anoxia) :
We then showed that LPS induced
HIF-1alpha mRNA expression was
blocked by an antioxidant,
NADPH oxidase inhibitors, and siRNA of gp91phox, a subunit of NADPH oxidase ... Taken together, these results suggest that LPS induces
HIF-1alpha mRNA expression and
activation via
NADPH oxidase and Sp1 in BV2 microglia
Li et al., Diabetes 2010
:
Overexpression of
Nox4 increased basal level of ROS generation,
HIF-1alpha , and VEGF expression in RCECs ... Moreover, inhibition of
Nox4 attenuated hypoxia induced upregulation of
HIF-1alpha and high-glucose elicited phosphorylation of STAT3
Diebold et al., Mol Biol Cell 2010
:
This response was dependent on the hypoxia-inducible transcription factor HIF-1alpha because overexpression of
HIF-1alpha increased
NOX4 expression, whereas HIF-1alpha depletion prevented this response ... Mutation of a putative hypoxia-responsive element in the NOX4 promoter abolished hypoxic and
HIF-1alpha induced activation of the
NOX4 promoter ...
Induction of
NOX4 by
HIF-1alpha contributed to maintain ROS levels after hypoxia and hypoxia induced proliferation of PASMCs