The gene PDE3A (phosphodiesterase 3A) encodes a cyclic nucleotide phosphodiesterase that is expressed mainly in cardiac and vascular myocytes and platelets. The cDNA contains a C-terminal catalytic region that spans around 280 amino acids and two hydrophobic regions at the N-terminus that participate in intracellular targeting. The gene containing 16 exons spanning over 130kb is mapped to human chromosome 12p12.
Synonyms: Anti-CGI-PDE A; Anti-Cyclic GMP-inhibited phosphodiesterase A; Anti-cGMP-inhibited 3',5'-cyclic phosphodiesterase A
Storage: -20C
Application: All Prestige Antibodies Powered by Atlas Antibodies are developed and validated by the Human Protein Atlas (HPA) project (www.proteinatlas.org)and as a result, are supported by the most extensive characterization in the industry. The Human Protein Atlas project can be subdivided into three efforts: Human Tissue Atlas, Cancer Atlas, and Human Cell Atlas. The antibodies that have been generated in support of the Tissue and Cancer Atlas projects have been tested by immunohistochemistry against hundreds of normal and disease tissues and through the recent efforts of the Human Cell Atlas project, many have been characterized by immunofluorescence to map the human proteome not only at the tissue level but now at the subcellular level. These images and the collection of this vast data set can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. To view these protocols and other useful information about Prestige Antibodies and the HPA, visit sigma.com/prestige.
Biochem Physiol Actions: The cyclic nucleotide PDEs (phosphodiesterases) hydrolyze cyclic nucleotides, cAMP and cGMP. The isoforms of PDE3 are cGMP-inhibited phosphodiesterases that hydrolyze cAMP and participate in the regulation of myocardial contractility, aggregation of platelets, and vascular smooth muscle relaxation. PDE3A activity is crucial for the maintenance of low equilibrium levels of cAMP and to determine the onset for platelet activation. Its activity can be increased by PKC (protein kinase C)-mediated phosphorylation, in turn regulating cAMP levels in human platelets.
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