Knockout of the cytochrome P450 reductase by CRISPR/Cas9 technology (POR(-/-)) in HEK293 cells overexpressing Nox4 or Nox5 did not interfere with ROS production in intact cells. However POR(-/-) abolished the signal in NADPH-stimulated assays using membrane fractions from the very same cells. Moreover membranes of rat smooth muscle cells treated with angiotensin II showed an increased NADPH-dependent signal with lucigen
this study provides novel insights into the regulation of gap junction function by CYPOR and suggests that Cx43 may play an important role(s) in CYPOR-mediated bone defects seen in patients.
The hepatic deficiency of this enzyme reverberates throughout the biological system and produces a coordinated response to the low levels of circulating cholesterol and bile.
POR function is indispensable for the proper regulation of retinoic acid levels and tissue distribution not only during early embryonic development but also in later morphogenesis and molecular patterning of the brain abdominal/caudal region and limbs.
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