Gs alpha subunit
GNAS complex locus | |
---|---|
Identifiers | |
Symbol | GNAS |
Alt. symbols | GNAS1 |
Entrez | 2778 |
HUGO | 4392 |
OMIM | 139320 |
RefSeq | NM_000516 |
UniProt | Q5JWF2 |
Other data | |
Locus | Chr. 20 q13.2-13.3 |
The Gs alpha subunit (Gαs, Gsα, or Gs protein) is a heterotrimeric G protein subunit that activates the cAMP-dependent pathway by activating adenylyl cyclase. It is one of the three main families of G proteins: Gαi/Gαo, Gαq, and Gαs.[1] A mnemonic for remembering this subunit is to look at the first letter (Gαs = Adenylate Cyclase stimulator).
Contents
1 Receptors
2 Function
3 See also
4 References
5 External links
Receptors
The G protein-coupled receptors that couple to this kind of G-protein include:
5-HT receptors types 5-HT4 and 5-HT7
ACTH receptor a.k.a. MC2R
Adenosine receptor types A2a and A2b
- Arginine vasopressin receptor 2
β-adrenergic receptors types β1, β2 and β3
- Calcitonin receptor
- Calcitonin gene-related peptide receptor
- Corticotropin-releasing hormone receptor
Dopamine receptors D1-like family (D1 and D5)- FSH-receptor
- Gastric inhibitory polypeptide receptor
- Glucagon receptor
- Growth-hormone-releasing hormone receptor
- Histamine H2 receptor
- Luteinizing hormone/choriogonadotropin receptor
Melanocortin receptor: MC1R, MC2R (a.k.a. ACTH receptor), MC3R, MC4R, MC5R
- Parathyroid hormone receptor 1
Prostaglandin receptor types D2 and I2
- Secretin receptor
- Thyrotropin receptor
- Trace amine-associated receptor 1
Function
The general function of Gs is to activate adenylyl cyclase, which, in turn, produces cAMP, which, in turn activates cAMP-dependent protein kinase. Further effects of Gs are thus found in function of cAMP-dependent protein kinase.
It provides a step in signal transduction. Amplification of the signal occurs for instance because the receptor activates several Gs.[2] However, each Gs activates only one adenylate cyclase.[2]
See also
- Second messenger system
References
^ Ellis C, Nature Reviews Drug Discovery GPCR Questionnaire Participants (July 2004). "The state of GPCR research in 2004". Nature Reviews. Drug Discovery. 3 (7): 575, 577–626. doi:10.1038/nrd1458. PMID 15272499..mw-parser-output cite.citation{font-style:inherit}.mw-parser-output q{quotes:"""""""'""'"}.mw-parser-output code.cs1-code{color:inherit;background:inherit;border:inherit;padding:inherit}.mw-parser-output .cs1-lock-free a{background:url("//upload.wikimedia.org/wikipedia/commons/thumb/6/65/Lock-green.svg/9px-Lock-green.svg.png")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-limited a,.mw-parser-output .cs1-lock-registration a{background:url("//upload.wikimedia.org/wikipedia/commons/thumb/d/d6/Lock-gray-alt-2.svg/9px-Lock-gray-alt-2.svg.png")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-subscription a{background:url("//upload.wikimedia.org/wikipedia/commons/thumb/a/aa/Lock-red-alt-2.svg/9px-Lock-red-alt-2.svg.png")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration{color:#555}.mw-parser-output .cs1-subscription span,.mw-parser-output .cs1-registration span{border-bottom:1px dotted;cursor:help}.mw-parser-output .cs1-hidden-error{display:none;font-size:100%}.mw-parser-output .cs1-visible-error{font-size:100%}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration,.mw-parser-output .cs1-format{font-size:95%}.mw-parser-output .cs1-kern-left,.mw-parser-output .cs1-kern-wl-left{padding-left:0.2em}.mw-parser-output .cs1-kern-right,.mw-parser-output .cs1-kern-wl-right{padding-right:0.2em}
^ ab Purves D, Augustine GJ, Fitzpatrick D, Hall WC, LaMantia AS, White LE, eds. (2007). Neuroscience (4th ed.). New York: W. H. Freeman. p. 155. ISBN 978-0-87893-697-7.
External links
G(s)alpha at the US National Library of Medicine Medical Subject Headings (MeSH)
GNAS+protein,+human at the US National Library of Medicine Medical Subject Headings (MeSH)
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