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Protein-coding gene in the species Homo sapiens

RGS4

RGS4
All data from the card 17
Aliases
RGS4, Rgs4, AA004315, AA597169, ESTM48, ESTM50, RGP4, SCZD9, regulator of G-protein signaling 4, regulator of G protein signaling 4
External IDs
OMIM: 602516; MGI: 108409; GeneCards: RGS4
Chr.
Chromosome 1 (human)
Band
1q23.3
End
163,076,802 bp
Chr.
Chromosome 1 (mouse)
Band
1 H2.3|1 76.84 cM
End
169,575,211 bp
BioGPS
More reference expression data
Databases
NCBI: entry; OMA: entry
Species
Human
Entrez
5999
Ensembl
ENSG00000117152
UniProt
P49798
RefSeq (mRNA)
NM_001102445NM_001113380NM_001113381NM_005613
RefSeq (protein)
NP_001095915NP_001106851NP_001106852NP_005604NP_005604.1
Location (UCSC)
Chr 1: 163.07 – 163.08 Mb

Regulator of G protein signaling 4 also known as RGP4 is a protein that in humans is encoded by the RGS4 gene. RGP4 regulates G protein signaling.

Function

Regulator of G protein signalling (RGS) family members are regulatory molecules that act as GTPase activating proteins (GAPs) for G alpha subunits of heterotrimeric G proteins. RGS proteins are able to deactivate G protein subunits of the Gi alpha, Go alpha and Gq alpha subtypes. They drive G proteins into their inactive GDP-bound forms. Regulator of G protein signaling 4 belongs to this family. All RGS proteins share a conserved 120-amino acid sequence termed the RGS domain which conveys GAP activity. Regulator of G protein signaling 4 protein is 37% identical to RGS1 and 97% identical to rat Rgs4. This protein negatively regulates signaling upstream or at the level of the heterotrimeric G protein and is localized in the cytoplasm.

Clinical significance

A number of studies associate the RGS4 gene with schizophrenia, while some fail to detect an association.

RGS4 is also of interest as one of the three main RGS proteins (along with RGS9 and RGS17) involved in terminating signalling by the mu opioid receptor, and may be important in the development of tolerance to opioid drugs.

Interactions

RGS4 has been shown to interact with:

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Text from Wikipedia, CC BY-SA 4.0 · Source article