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cGMP-dependent protein kinase or protein kinase G (PKG) is a serine/threonine-specific protein kinase that is activated by cGMP. It phosphorylates a number of biologically important targets and is implicated in the regulation of smooth muscle relaxation, platelet function, sperm metabolism, cell division, and nucleic acid synthesis.
Elevated cGMP levels then lead to the activation of some protein-dependent kinases like PKG. [5] For example, PKG (protein kinase G) is a dimer consisting of one catalytic and one regulatory unit, with the regulatory units blocking the active sites of the catalytic units.
PK-G: Protein kinase G (cGMP-dependent). PDE3 is a phosphodiesterase . The PDEs belong to at least eleven related gene families , which are different in their primary structure , substrate affinity , responses to effectors , and regulation mechanism .
cGMP-dependent protein kinase 1, alpha isozyme is an enzyme that in humans is encoded by the PRKG1 gene. [5] [6] [7] Interactions. PRKG1 has been shown to interact with:
In cell biology, protein kinase A (PKA) is a family of serine-threonine kinase [1] whose activity is dependent on cellular levels of cyclic AMP (cAMP). PKA is also known as cAMP-dependent protein kinase ( EC 2.7.11.11 ).
The receptor changes conformation and transmits a signal that activates an enzyme in the cell membrane interior called adenylyl cyclase. This releases cAMP into the cell interior, where it stimulates a protein kinase called cyclic AMP-dependent protein kinase. By phosphorylating proteins, cyclic AMP-dependent protein kinase alters protein activity.
The enzyme 3′,5′-cyclic-GMP phosphodiesterase (EC 3.1.4.35) catalyzes the reaction guanosine 3′,5′-cyclic phosphate + H 2 O ⇌ {\displaystyle \rightleftharpoons } guanosine 5′-phosphate This enzyme belongs to the family of hydrolases , specifically those acting on phosphoric diester bonds.
cGMP will then stimulate cGMP-dependent protein kinase (PKG), which will then induce smooth muscle relaxation. This is particularly important in the vasculature, where vascular smooth muscle will bind ANP released as a result of increasing right atrial pressure and will cause the walls of the vasculature to relax.
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