| Primary Identifier | IPR001856 | Type | Family |
| Short Name | Somatstn_rcpt_3 |
| description | Somatostatin (SST), also known as somatotropin release-inhibiting factor (SRIF), is a hypothalamic hormone, a pancreatic hormone, and a central and peripheral neurotransmitter. Somatostatin has a wide distribution throughout the central nervous system (CNS) as well as in peripheral tissues, for example in the pituitary, pancreas and stomach. The various actions of somatostatin are mediated by a family of rhodopsin-like G protein-coupled receptors, which comprise of five distinct subtypes: Somatostatin receptor 1 (SSTR1), Somatostatin receptor 2 (SSTR2), Somatostatin receptor 3 (SSTR3), Somatostatin receptor 4 (SSTR4) and Somatostatin receptor 5 (SSTR5) [, , ]. These subtypes are widely expressed in many tissues [, , , , , ], and frequently multiple subtypes coexist in the same cell []. The somatostatin receptor subtypes also share common signalling pathways, such as the inhibition of adenylyl cyclase [, ], activation of phosphotyrosine phosphatase (PTP), and modulation of mitogen-activated protein kinase (MAPK) through G protein-dependent mechanisms. Some of the subtypes are also coupled to inward rectifying K+ channels (SSTR2, SSTR3, SSTR4, SSTR5) [, ], to voltage-dependent Ca2+ channels (SSTR1, SSTR2) [], to an Na+/H+ exchanger (SSTR1), AMPA/kainate glutamate channels (SSTR1, SSTR2), phospholipase C (SSTR2, SSTR5), and phospholipase A2 (SSTR4) []. Amongst the wide spectrum of somatostatin effects, several biological responses have been identified that display absolute or relative subtype selectivity. These include GH secretion (SSTR2 and 5), insulin secretion (SSTR5), glucagon secretion (SSTR2), and immune responses (SSTR2) [].This entry represents SSTR3. It is widely distributed in mouse brain, with high levels in the forebrain, hippocampus and amygdala; moderate levels are also present in the substantia nigra. All five human somatostatin receptors expressed in COS-7 cells are coupled to activation of phosphoinositide (PI)-specific PLC-beta; and Ca2+ mobilisation via pertussis toxin-sensitive G protein(s) with an order of potency of SSTR5 >SSTR2 >SSTR3 >SSTR4 >SSTR1 []. Inhibition of angiogenesis has been shown to be via the SSTR3, and involves the inhibition of MAPK and endothelial nitric oxide synthase (eNOS) activity []. |
