ARHGAP25

From Wikipedia, the free encyclopedia
ARHGAP25
Available structures
PDBOrtholog search: PDBe RCSB
Identifiers
AliasesARHGAP25, HEL-S-308, KAIA0053, Rho GTPase activating protein 25
External IDsOMIM: 610587 MGI: 2443687 HomoloGene: 45507 GeneCards: ARHGAP25
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_001037727
NM_001286610
NM_175476

RefSeq (protein)

NP_001032816
NP_001273539
NP_780685

Location (UCSC)Chr 2: 68.68 – 68.83 MbChr 6: 87.44 – 87.51 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Rho GTPase activating protein 25 is a protein that in humans is encoded by the ARHGAP25 gene.[5] The gene is also known as KAIA0053.[5] ARHGAP25 belongs to a family of Rho GTPase-modulating proteins that are implicated in actin remodeling, cell polarity, and cell migration.[6]

Model organisms[]

Model organisms have been used in the study of ARHGAP25 function. A conditional knockout mouse line, called Arhgap25tm1a(KOMP)Wtsi[13][14] was generated as part of the International Knockout Mouse Consortium program — a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists.[15][16][17]

Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.[11][18] Twenty-one tests were carried out on homozygous-mutant mice and one significant abnormality was observed: abnormal retina morphology and pigmentation.[11]

References[]

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000163219 - Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000030047 - 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. ^ a b "Rho GTPase activating protein 25". Retrieved 2011-12-05.
  6. ^ Katoh M, Katoh M (August 2004). "Identification and characterization of ARHGAP24 and ARHGAP25 genes in silico". International Journal of Molecular Medicine. 14 (2): 333–8. doi:10.3892/ijmm.14.2.333. PMID 15254788.
  7. ^ "Eye morphology data for Arhgap25". Wellcome Trust Sanger Institute.
  8. ^ "Clinical chemistry data for Arhgap25". Wellcome Trust Sanger Institute.
  9. ^ "Salmonella infection data for Arhgap25". Wellcome Trust Sanger Institute.
  10. ^ "Citrobacter infection data for Arhgap25". Wellcome Trust Sanger Institute.
  11. ^ a b c Gerdin AK (2010). "The Sanger Mouse Genetics Programme: High throughput characterisation of knockout mice". Acta Ophthalmologica. 88: 925–7. doi:10.1111/j.1755-3768.2010.4142.x. S2CID 85911512.
  12. ^ Mouse Resources Portal, Wellcome Trust Sanger Institute.
  13. ^ "International Knockout Mouse Consortium".
  14. ^ "Mouse Genome Informatics".
  15. ^ Skarnes WC, Rosen B, West AP, Koutsourakis M, Bushell W, Iyer V, Mujica AO, Thomas M, Harrow J, Cox T, Jackson D, Severin J, Biggs P, Fu J, Nefedov M, de Jong PJ, Stewart AF, Bradley A (June 2011). "A conditional knockout resource for the genome-wide study of mouse gene function". Nature. 474 (7351): 337–42. doi:10.1038/nature10163. PMC 3572410. PMID 21677750.
  16. ^ Dolgin E (June 2011). "Mouse library set to be knockout". Nature. 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718.
  17. ^ Collins FS, Rossant J, Wurst W (January 2007). "A mouse for all reasons". Cell. 128 (1): 9–13. doi:10.1016/j.cell.2006.12.018. PMID 17218247. S2CID 18872015.
  18. ^ van der Weyden L, White JK, Adams DJ, Logan DW (June 2011). "The mouse genetics toolkit: revealing function and mechanism". Genome Biology. 12 (6): 224. doi:10.1186/gb-2011-12-6-224. PMC 3218837. PMID 21722353.

Further reading[]

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