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
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