Somatostatin receptor 3
Somatostatin Receptor 3[edit | edit source]
Somatostatin receptor 3 (SSTR3) is a G protein-coupled receptor that binds the peptide hormone somatostatin. It is one of the five known somatostatin receptors, which are involved in a variety of physiological processes including neurotransmission, cell proliferation, and endocrine signaling.
Structure[edit | edit source]
SSTR3 is a member of the G protein-coupled receptor (GPCR) superfamily, characterized by seven transmembrane domains. The receptor is encoded by the SSTR3 gene located on chromosome 22 in humans. The structure of SSTR3 allows it to interact with G proteins, which are intracellular proteins that mediate signal transduction from the receptor to various downstream effectors.
Function[edit | edit source]
The primary function of SSTR3 is to mediate the effects of somatostatin, a hormone that inhibits the release of several other hormones such as growth hormone, insulin, and glucagon. SSTR3 is involved in the regulation of neuroendocrine and exocrine secretions, as well as in the modulation of neurotransmitter release in the central nervous system.
Expression[edit | edit source]
SSTR3 is expressed in various tissues throughout the body, including the brain, pancreas, and gastrointestinal tract. Its expression pattern suggests a role in both central and peripheral physiological processes.
Clinical Significance[edit | edit source]
Alterations in SSTR3 expression or function have been implicated in several diseases, including neuroendocrine tumors, Alzheimer's disease, and diabetes mellitus. SSTR3 is a potential target for therapeutic agents designed to modulate somatostatin signaling in these conditions.
Research[edit | edit source]
Ongoing research is focused on understanding the precise role of SSTR3 in health and disease, as well as developing selective agonists and antagonists that can modulate its activity. Such compounds could have therapeutic potential in treating disorders associated with dysregulated somatostatin signaling.
See Also[edit | edit source]
References[edit | edit source]
External Links[edit | edit source]
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