![]() There are three main effectors of cAMP: PKA, the guanine-nucleotide-exchange factor (GEF) EPAC and cyclic-nucleotide-gated ion channels. Crosstalk with other pathways provides further modulation of the signal strength and cell-type specificity, and feedforward signaling by PKA itself stimulates PDE4. 2), such as calcium signaling (through calmodulin, CamKII, CamKIV, and calcineurin ), subunits of other G proteins (e.g., α i, α o, and α q proteins, and the βγ subunits in some cases), inositol lipids (by PKC), and receptor tyrosine kinases (through the ERK MAP kinase and PKB) ( Yoshimasa et al. Indeed both ACs and PDEs are regulated positively and negatively by numerous other signaling pathways (see Fig. ![]() 2002).Īlternatively, AC activity can be inhibited by ligands that stimulate GPCRs coupled to G i and/or cAMP can be degraded by PDEs. cAMP generated as a consequence of AC activation can activate several effectors, the most well studied of which is cAMP-dependent protein kinase (PKA) ( Pierce et al. ![]() The βγ subunits can also stimulate some AC isoforms. α s is released from heterotrimeric αβγ G-protein complexes following binding of agonist ligands to GPCRs (e.g., epinephrine in the case of β adrenoceptors) and binds to and activates AC. Most ACs (soluble bicarbonate-regulated ACs are the exception) are activated downstream from G-protein-coupled receptors (GPCRs) such as the β adrenoceptor by interactions with the α subunit of the G s protein (α s). ![]()
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