Title : Exogenous nitric oxide generates ROS and induces cardioprotection: involvement of PKG, mitochondrial KATP channels, and ERK.

Pub. Date : 2004 Apr

PMID : 14656708






7 Functional Relationships(s)
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1 Exogenous nitric oxide generates ROS and induces cardioprotection: involvement of PKG, mitochondrial KATP channels, and ERK. Reactive Oxygen Species protein kinase cGMP-dependent 1 Homo sapiens
2 We examined whether cGMP-dependent protein kinase (PKG) and mitochondrial ATP-sensitive potassium (K(ATP)) channels are involved in S-nitroso-N-acetyl penicillamine (SNAP)-induced reactive oxygen species (ROS) generation. Reactive Oxygen Species protein kinase cGMP-dependent 1 Homo sapiens
3 KT-5823, an inhibitor of PKG, prevented ROS generation, indicating that PKG is required for ROS generation. Reactive Oxygen Species protein kinase cGMP-dependent 1 Homo sapiens
4 KT-5823, an inhibitor of PKG, prevented ROS generation, indicating that PKG is required for ROS generation. Reactive Oxygen Species protein kinase cGMP-dependent 1 Homo sapiens
5 KT-5823, an inhibitor of PKG, prevented ROS generation, indicating that PKG is required for ROS generation. Reactive Oxygen Species protein kinase cGMP-dependent 1 Homo sapiens
6 In addition, 8-bromoguanosine 3",5"-cyclic monophosphate (8-BrcGMP), an activator of PKG, induced ROS generation. Reactive Oxygen Species protein kinase cGMP-dependent 1 Homo sapiens
7 These results suggest that SNAP-induced ROS generation is mediated by activation of PKG and mitochondrial K(ATP) channels and that opening of mitochondrial K(ATP) channels is the downstream event of PKG activation. Reactive Oxygen Species protein kinase cGMP-dependent 1 Homo sapiens