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CALM3 — NOX4

Text-mined interactions from Literome

Sterner-Kock et al., J Leukoc Biol 1999 (Inflammation) : Our results indicate that SP primes two distinct pathways with respect to the induction of reactive oxygen species in the human neutrophil : the production of superoxide anion and hydrogen peroxide by the calmodulin dependent NADPH oxidase , and the generation of NO by a constitutive NO synthase
Mayer et al., FEBS Lett 1991 : We found that the purified enzyme also contains FAD, FMN and non-heme iron in equimolar amounts and exhibits striking activities, including a Ca2+/calmodulin dependent NADPH oxidase activity, leading to the formation of hydrogen peroxide at suboptimal concentrations of L-arginine or H4biopterin
Savitha et al., Cell Signal 1990 : Kinetics of capsaicin uptake by macrophages ( 10 ( 3 ) cells ) revealed that a maximum of 200 microM capsaicin was taken up within 10 min. Ca2+ ionophore triggered generation of superoxide anion and hydrogen peroxide by macrophages was inhibited in a dose dependent manner by fluphenazine ( IC50, 20 microM and 12 microM, respectively ) and also by capsaicin ( IC50, 30 microM and 9 microM, respectively ), suggesting an involvement of calmodulin in the regulation of NADPH oxidase
Sakata et al., Biochem Biophys Res Commun 1987 : Calmodulin inhibitors, W-7 and TFP, block the calmodulin independent activation of NADPH-oxidase by arachidonate in a cell-free system ... The calmodulin inhibitor, N- ( 6-aminohexyl ) -5-chloro-1-naphthalene sulfonamide ( W-7 ), or trifluoperazine inhibited not only Fc gamma-receptor mediated cytosolic free Ca2+ increase and O2- generation in macrophages, but also an arachidonate induced activation of NADPH-oxidase in a cell-free system
Jones et al., Biochim Biophys Acta 1982 : Calmodulin dependent stimulation of the NADPH oxidase of human neutrophils ... These studies suggest a role for calmodulin in the control of NADPH oxidase but that calmodulin alone is not sufficient for activation
Hirata et al., J Clin Invest 1993 : ETB agonist induced NOx production was blocked by a calmodulin inhibitor and an intracellular Ca2+ chelator, but not by an extracellular Ca2+ chelator or a Ca2+ channel blocker