Rho GTPase-activating protein 21

ARHGAP21
Identifiers
AliasesARHGAP21, ARHGAP10, Rho GTPase activating protein 21
External IDsOMIM: 609870; MGI: 1918685; GeneCards: ARHGAP21
Available structures
PDBOrtholog search: PDBe RCSB
Orthologs
DatabasesNCBI: entry; OMA: entry
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_020824

NM_001081364
NM_001128084

RefSeq (protein)
Location (UCSC)Chr 10: 24.58 – 24.72 MbChr 2: 20.85 – 20.97 Mb
PubMed search
Wikidata
View/Edit HumanView/Edit Mouse

Rho GTPase activating protein 21 is a protein that in humans is encoded by the ARHGAP21 gene.

Function

ARHGAP21 functions preferentially as a GTPase-activating protein (GAP) for CDC42 (MIM 116952) and regulates the ARP2/3 complex (MIM 604221) and F-actin dynamics at the Golgi through control of CDC42 activity. There is little scientific literature on ARHGAP21, but recent reviews highlighted that it plays an important role in cytoskeletal processes in cancer, substance transport within the cell, and insulin secretion

References

  1. 1 2 3 GRCh38: Ensembl release 89: ENSG00000107863 – Ensembl, May 2017
  2. 1 2 3 GRCm38: Ensembl release 89: ENSMUSG00000036591 – 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. ↑ "Entrez Gene: Rho GTPase activating protein 21". Retrieved 2017-01-30.
  6. ↑ Dubois T, Paléotti O, Mironov AA, Fraisier V, Stradal TE, De Matteis MA, et al. (2005). "Golgi-localized GAP for Cdc42 functions downstream of ARF1 to control Arp2/3 complex and F-actin dynamics". Nature Cell Biology. 7 (4): 353–364. doi:10.1038/ncb1244. PMID 15793564. S2CID 37000096.
  7. ↑ Rosa LR, Soares GM, Silveira LR, Boschero AC, Barbosa-Sampaio HC (November 2018). "ARHGAP21 as a master regulator of multiple cellular processes". Journal of Cellular Physiology. 233 (11): 8477–8481. doi:10.1002/jcp.26829. PMID 29856495. S2CID 46919924.

Further reading

This article incorporates text from the United States National Library of Medicine, which is in the public domain.