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
we observed that miR-378 modulates the oscillation amplitudes of Cdkn1a in the control of cell cycle and Por in the regulation of oxidation reduction by forming partnership with different circadian transcription factors
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.
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