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Rho GTPase activating protein 25 is a protein that in humans is encoded by the ARHGAP25 gene.[1] The gene is also known as KAIA0053.[1] ARHGAP25 belongs to a family of Rho GTPase-modulating proteins that are implicated in actin remodeling, cell polarity, and cell migration.[2]

Model organisms[edit]

Model organisms have been used in the study of ARHGAP25 function. A conditional knockout mouse line, called Arhgap25tm1a(KOMP)Wtsi[9][10] 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.[11][12][13]

Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.[7][14] Twenty-one tests were carried out on homozygous-mutant mice and one significant abnormality was observed: abnormal retina morphology and pigmentation.[7]


  1. ^ a b "Rho GTPase activating protein 25". Retrieved 2011-12-05. 
  2. ^ Katoh, M.; Katoh, M. (2004). "Identification and characterization of ARHGAP24 and ARHGAP25 genes in silico". International journal of molecular medicine. 14 (2): 333–338. doi:10.3892/ijmm.14.2.333. PMID 15254788. 
  3. ^ "Eye morphology data for Arhgap25". Wellcome Trust Sanger Institute. 
  4. ^ "Clinical chemistry data for Arhgap25". Wellcome Trust Sanger Institute. 
  5. ^ "Salmonella infection data for Arhgap25". Wellcome Trust Sanger Institute. 
  6. ^ "Citrobacter infection data for Arhgap25". Wellcome Trust Sanger Institute. 
  7. ^ 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. 
  8. ^ Mouse Resources Portal, Wellcome Trust Sanger Institute.
  9. ^ "International Knockout Mouse Consortium". 
  10. ^ "Mouse Genome Informatics". 
  11. ^ Skarnes, W. C.; Rosen, B.; West, A. P.; Koutsourakis, M.; Bushell, W.; Iyer, V.; Mujica, A. O.; Thomas, M.; Harrow, J.; Cox, T.; Jackson, D.; Severin, J.; Biggs, P.; Fu, J.; Nefedov, M.; De Jong, P. J.; Stewart, A. F.; Bradley, A. (2011). "A conditional knockout resource for the genome-wide study of mouse gene function". Nature. 474 (7351): 337–342. doi:10.1038/nature10163. PMC 3572410Freely accessible. PMID 21677750. 
  12. ^ Dolgin E (2011). "Mouse library set to be knockout". Nature. 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718. 
  13. ^ Collins FS, Rossant J, Wurst W (2007). "A Mouse for All Reasons". Cell. 128 (1): 9–13. doi:10.1016/j.cell.2006.12.018. PMID 17218247. 
  14. ^ van der Weyden L, White JK, Adams DJ, Logan DW (2011). "The mouse genetics toolkit: revealing function and mechanism.". Genome Biol. 12 (6): 224. doi:10.1186/gb-2011-12-6-224. PMC 3218837Freely accessible. PMID 21722353. 

Further reading[edit]

  • Takefuji, M.; Asano, H.; Mori, K.; Amano, M.; Kato, K.; Watanabe, T.; Morita, Y.; Katsumi, A.; Itoh, T.; Takenawa, T.; Hirashiki, A.; Izawa, H.; Nagata, K.; Hirayama, H.; Takatsu, F.; Naoe, T.; Yokota, M.; Kaibuchi, K. (2009). "Mutation of ARHGAP9 in patients with coronary spastic angina". Journal of Human Genetics. 55 (1): 42–49. doi:10.1038/jhg.2009.120. PMID 19911011. 
  • Nomura, N.; Nagase, T.; Miyajima, N.; Sazuka, T.; Tanaka, A.; Sato, S.; Seki, N.; Kawarabayasi, Y.; Ishikawa, K.; Tabata, S. (1994). "Prediction of the coding sequences of unidentified human genes. II. The coding sequences of 40 new genes (KIAA0041-KIAA0080) deduced by analysis of cDNA clones from human cell line KG-1". DNA research : an international journal for rapid publication of reports on genes and genomes. 1 (5): 223–229. doi:10.1093/dnares/1.5.223. PMID 7584044.