Induction of Endothelial NO Synthase by Hydrogen Peroxide via a Ca 2+ /Calmodulin-Dependent Protein Kinase II/Janus Kinase 2–Dependent Pathway

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Induction of endothelial NO synthase by hydrogen peroxide via a Ca(2+)/calmodulin-dependent protein kinase II/janus kinase 2-dependent pathway.

We have recently demonstrated that hydrogen peroxide (H(2)O(2)) is an extremely potent stimulus of endothelial NO synthase (eNOS) gene expression. The present study was designed to identify the signaling mechanisms mediating this response. Induction of eNOS expression by H(2)O(2) was found to be Ca(2+) dependent, inasmuch as it was blocked by BAPTA-AM. Further studies have indicated that Ca(2+)...

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Induction of Endothelial NO Synthase by Hydrogen Peroxide via a Ca/Calmodulin-Dependent Protein Kinase II/Janus Kinase 2–Dependent Pathway

We have recently demonstrated that hydrogen peroxide (H2O2) is an extremely potent stimulus of endothelial NO synthase (eNOS) gene expression. The present study was designed to identify the signaling mechanisms mediating this response. Induction of eNOS expression by H2O2 was found to be Ca 21 dependent, inasmuch as it was blocked by BAPTA-AM. Further studies have indicated that Ca/calmodulin-d...

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A Brain - specific Ca 2 + / Calmodulin - dependent Protein Kinase ( CaM Kinase - Gr ) Is Regulated by Autophosphorylation

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Hydrogen peroxide activates endothelial nitric-oxide synthase through coordinated phosphorylation and dephosphorylation via a phosphoinositide 3-kinase-dependent signaling pathway.

Endothelial nitric-oxide synthase (eNOS) is an important component of vascular homeostasis. During vascular disease, endothelial cells are exposed to excess reactive oxygen species that can alter cellular phenotype by inducing various signaling pathways. In the current study, we examined the implications of H(2)O(2)-induced signaling for eNOS phosphorylation status and activity in porcine aorti...

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Ca 2 - Calmodulin - dependent Protein Kinase II Potentiates

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ژورنال

عنوان ژورنال: Arteriosclerosis, Thrombosis, and Vascular Biology

سال: 2001

ISSN: 1079-5642,1524-4636

DOI: 10.1161/hq1001.097028