Human Gene RGS4 (ENST00000421743.6) from GENCODE V44
Description: Homo sapiens regulator of G protein signaling 4 (RGS4), transcript variant 1, mRNA. (from RefSeq NM_001102445) RefSeq Summary (NM_001102445): Regulator of G protein signaling (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. Regulator of G protein signaling 4 protein is 37% identical to RGS1 and 97% identical to rat Rgs4. This protein negatively regulate signaling upstream or at the level of the heterotrimeric G protein and is localized in the cytoplasm. Alternatively spliced transcript variants have been found for this gene. [provided by RefSeq, Jul 2008]. Gencode Transcript: ENST00000421743.6 Gencode Gene: ENSG00000117152.14 Transcript (Including UTRs) Position: hg38 chr1:163,068,775-163,076,802 Size: 8,028 Total Exon Count: 6 Strand: + Coding Region Position: hg38 chr1:163,068,935-163,074,560 Size: 5,626 Coding Exon Count: 6
ID:RGS4_HUMAN DESCRIPTION: RecName: Full=Regulator of G-protein signaling 4; Short=RGP4; Short=RGS4; FUNCTION: Inhibits signal transduction by increasing the GTPase activity of G protein alpha subunits thereby driving them into their inactive GDP-bound form. Activity on G(z)-alpha is inhibited by phosphorylation of the G-protein. Activity on G(z)-alpha and G(i)-alpha-1 is inhibited by palmitoylation of the G-protein. TISSUE SPECIFICITY: Expressed in brain and heart. Expressed in brain at protein level. Expressed in prefontal and visual cortex. Isoform 4 and isoform 5 are expressed ubiquitously. Isoform 1, isoform 2 and isoform 3 are not expressed in the cerebellum. PTM: Palmitoylated on Cys-2 and/or Cys-12. PTM: Phosphorylated by cyclic GMP-dependent protein kinase (By similarity). DISEASE: Genetic variation in RGS4 is associated with susceptibility to schizophrenia type 9 (SCZD9) [MIM:604906]. A complex, multifactorial psychotic disorder or group of disorders characterized by disturbances in the form and content of thought (e.g. delusions, hallucinations), in mood (e.g. inappropriate affect), in sense of self and relationship to the external world (e.g. loss of ego boundaries, withdrawal), and in behavior (e.g bizarre or apparently purposeless behavior). Although it affects emotions, it is distinguished from mood disorders in which such disturbances are primary. Similarly, there may be mild impairment of cognitive function, and it is distinguished from the dementias in which disturbed cognitive function is considered primary. Some patients manifest schizophrenic as well as bipolar disorder symptoms and are often given the diagnosis of schizoaffective disorder. SIMILARITY: Contains 1 RGS domain.
The RNAfold program from the Vienna RNA Package is used to perform the secondary structure predictions and folding calculations. The estimated folding energy is in kcal/mol. The more negative the energy, the more secondary structure the RNA is likely to have.
Pfam Domains: PF00615 - Regulator of G protein signaling domain
ModBase Predicted Comparative 3D Structure on P49798
Front
Top
Side
The pictures above may be empty if there is no ModBase structure for the protein. The ModBase structure frequently covers just a fragment of the protein. You may be asked to log onto ModBase the first time you click on the pictures. It is simplest after logging in to just click on the picture again to get to the specific info on that model.
Orthologous Genes in Other Species
Orthologies between human, mouse, and rat are computed by taking the best BLASTP hit, and filtering out non-syntenic hits. For more distant species reciprocal-best BLASTP hits are used. Note that the absence of an ortholog in the table below may reflect incomplete annotations in the other species rather than a true absence of the orthologous gene.