Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.11.12 (PKG)
2,515 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cyclic GMP mediates vascular smooth muscle relaxation to a variety of drugs and naturally-occurring substances. The reduction of intracellular Ca2+ levels is believed to underlie this action, but the mechanism of this effect is unknown. In order to test the hypothesis that inhibition of guanine nucleotide-binding protein function is involved in the actions of cGMP, the effects of cGMP-dependent protein kinase on the phosphorylation of both pertussis toxin-sensitive (Gi/Go) and insensitive (Gz) G-proteins were examined in vitro. None of these proteins were effective substrates for either cGMP- or cAMP-dependent protein kinases, despite the fact that assay conditions were designed to detect poorly phosphorylated substrate proteins. In line with these observations, atriopeptin II did not inhibit angiotensin II-treated inositol phosphate formation in cultured vascular smooth muscle cells. These results suggest that phosphorylation by cGMP-dependent protein kinase of these G-proteins is not the major mechanism by which cGMP reduces intracellular Ca2+ levels in vascular smooth muscle.
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PMID:Pertussis toxin-sensitive and insensitive guanine nucleotide binding proteins (G-proteins) are not phosphorylated by cyclic GMP-dependent protein kinase. 183 99