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ATP5O — CPN1

Text-mined interactions from Literome

Vaziri et al., J Hypertens Suppl 2002 (Hypertension) : Several mechanisms have been shown to contribute to the pathogenesis of lead induced hypertension : ( 1 ) avid oxidation and inactivation of endogenous nitric oxide ( NO ) by reactive oxygen species leading to functional NO deficiency ; ( 2 ) increased sympathetic activity and circulating noradrenaline coupled with decreased vascular and elevated renal beta-adrenergic receptor density ; ( 3 ) increased angiotensin converting enzyme (ACE) activity and elevated plasma renin, angiotensin II and aldosterone levels ; ( 4 ) heightened kininase I and kininase II activities ; ( 5 ) possible increase in endothelin and thromboxane production ; and ( 6 ) lead mediated inhibition of vascular smooth muscle Na ( + ) -K+ ATPase leading to a rise in cellular Na+ and hence Ca2+ stores
Baneyx et al., J Biol Chem 1995 : Cpn21 also inhibits the ATPase activity of GroEL