GO6983

Description	Go 6983 (300 μM) suppresses PKCμ auto-phosphorylation by 20% reduction in NIH3T3 transfected with PKCμ. In hearts reperfused with PMNs and G? 6983 (100 nM), left ventricular developed pressure (LVD) and the rate of LVDP recoveres to 89% and 74% of baseline values, respectively, significantly higher than PMNs alone. G? 6983 (100 nM) significantly reduces PMNs adherence to the endothelium and infiltration into the myocardium compared with Ischemia followed by reperfusion (I/R)+ PMN hearts, and significantly inhibits superoxide release from PMNs by 90%. G? 6983 attenuates post-I/R cardiac contractile dysfunction in the presence of PMNs, which may be related in part to decreased superoxide production. G? 6983 significantly inhibits antigen-induced superoxide release from leukocytes of patients previously sensitized to tree pollen. Go 6983 inhibited intracellular Ca(2+) accumulation in human vascular tissue, suggesting a mechanism for its vasodilator properties. Go-6983 (1 μM) combined with
Pathways	TGF beta/Smad Epigenetics
Targets	PKC

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