Gs alpha subunit

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GNAS
Protein GNAS PDB 1azs.png
Identifiers
AliasesGNAS, AHO, C20orf45, GNAS1, GPSA, GSA, GSP, NESP, POH, SCG6, SgVI, GNAS complex locus, PITA3
External IDsOMIM: 139320 MGI: 95777 HomoloGene: 55534 GeneCards: GNAS
Gene location (Human)
Chromosome 20 (human)
Chr.Chromosome 20 (human)[1]
Chromosome 20 (human)
Genomic location for GNAS
Genomic location for GNAS
Band20q13.32Start58,839,718 bp[1]
End58,911,192 bp[1]
RNA expression pattern
PBB GE GNAS 200780 x at fs.png

PBB GE GNAS 200981 x at fs.png

PBB GE GNAS 211858 x at fs.png
More reference expression data
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)
RefSeq (protein)
Location (UCSC)Chr 20: 58.84 – 58.91 MbChr 2: 174.28 – 174.35 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

The Gs alpha subunit (Gαs, Gsα) is a subunit of the heterotrimeric G protein Gs that stimulates the cAMP-dependent pathway by activating adenylyl cyclase. Gsα is a GTPase that functions as a cellular signaling protein. Gsα is the founding member of one of the four families of heterotrimeric G proteins, defined by the alpha subunits they contain: the Gαs family, Gαi/Gαo family, Gαq family, and Gα12/Gα13 family.[5] The Gs-family has only two members: the other member is Golf, named for its predominant expression in the olfactory system. In humans, Gsα is encoded by the GNAS complex locus, while Golfα is encoded by the GNAL gene.

Function[edit]

The general function of Gs is to activate intracellular signaling pathways in response to activation of cell surface G protein-coupled receptors (GPCRs). GPCRs function as part of a three-component system of receptor-transducer-effector.[6][7] The transducer in this system is a heterotrimeric G protein, composed of three subunits: a Gα protein such as Gsα, and a complex of two tightly linked proteins called Gβ and Gγ in a Gβγ complex.[6][7] When not stimulated by a receptor, Gα is bound to GDP and to Gβγ to form the inactive G protein trimer.[6][7] When the receptor binds an activating ligand outside the cell (such as a hormone or neurotransmitter), the activated receptor acts as a guanine nucleotide exchange factor to promote GDP release from and GTP binding to Gα, which drives dissociation of GTP-bound Gα from Gβγ.[6][7] In particular, GTP-bound, activated Gsα binds to adenylyl cyclase to produce the second messenger cAMP, which in turn activates the cAMP-dependent protein kinase (also called Protein Kinase A or PKA).[6][7] Cellular effects of Gsα acting through PKA are described here.

Although each GTP-bound Gsα can activate only one adenylyl cyclase enzyme, amplification of the signal occurs because one receptor can activate multiple copies of Gs while that receptor remains bound to its activating agonist, and each Gsα-bound adenylyl cyclase enzyme can generate substantial cAMP to activate many copies of PKA.[8]

Receptors[edit]

The G protein-coupled receptors that couple to the Gs family proteins include:

See also[edit]

References[edit]

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000087460 - Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000027523 - Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^ 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.
  6. ^ a b c d e Gilman AG (1987). "G proteins: transducers of receptor-generated signals". Annual Review of Biochemistry. 56: 615–649. doi:10.1146/annurev.bi.56.070187.003151.
  7. ^ a b c d e Rodbell M (1995). "Nobel Lecture: Signal transduction: Evolution of an idea". Bioscience Reports. 15 (3): 117–133. doi:10.1007/bf01207453.
  8. ^ 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[edit]