Protein arginine methyltransferase 7 is a protein that in humans is encoded by the PRMT7 gene.[1] Arginine methylation is an apparently irreversible protein modification catalyzed by arginine methyltransferases, such as PMT7, using S-adenosylmethionine (AdoMet) as the methyl donor. Arginine methylation is implicated in signal transduction, RNA transport, and RNA splicing.[1][2]

Model organisms

Model organisms have been used in the study of PRMT7 function. A conditional knockout mouse line, called Prmt7tm1a(EUCOMM)Wtsi[7][8] 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.[9][10][11]

Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.[5][12] Twenty five tests were carried out on mutant mice and two significant abnormalities were observed.[5] Fewer than expected homozygous mutant mice survived until weaning and those that did survive displayed evidence of chromosomal instability in a micronucleus test.[5]

References

  1. 1 2 "Protein arginine methyltransferase 7". Retrieved 2011-12-06.
  2. ↑ Miranda, T. B.; Miranda, M.; Frankel, A.; Clarke, S. (2004). "PRMT7 is a Member of the Protein Arginine Methyltransferase Family with a Distinct Substrate Specificity". Journal of Biological Chemistry. 279 (22): 22902–22907. doi:10.1074/jbc.M312904200. PMID 15044439.
  3. ↑ "Salmonella infection data for Prmt7". Wellcome Trust Sanger Institute.
  4. ↑ "Citrobacter infection data for Prmt7". Wellcome Trust Sanger Institute.
  5. 1 2 3 4 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.
  6. ↑ Mouse Resources Portal, Wellcome Trust Sanger Institute.
  7. ↑ "International Knockout Mouse Consortium".
  8. ↑ "Mouse Genome Informatics".
  9. ↑ 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 3572410. PMID 21677750.
  10. ↑ Dolgin E (2011). "Mouse library set to be knockout". Nature. 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718.
  11. ↑ 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. S2CID 18872015.
  12. ↑ 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 3218837. PMID 21722353.{{cite journal}}: CS1 maint: unflagged free DOI (link)

Further reading


This article is issued from Wikipedia. The text is licensed under Creative Commons - Attribution - Sharealike. Additional terms may apply for the media files.