CRLF3
Cytokine receptor-like factor 3 is a protein that in humans is encoded by the CRLF3 gene.[3]
Model organisms
Model organisms have been used in the study of CRLF3 function. A conditional knockout mouse line, called Crlf3tm1a(KOMP)Wtsi[10][11] 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.[12][13][14] Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.[8][15] Twenty six tests were carried out and two significant phenotypes were reported. Homozygous mutant female adults had a significant increase in circulating levels of fructosamine, while mutants of both sexes had decreased platelet cell numbers.[8]
References
- ↑ "Human PubMed Reference:".
- ↑ "Mouse PubMed Reference:".
- ↑ "Entrez Gene: cytokine receptor-like factor 3".
- ↑ "Clinical chemistry data for Crlf3". Wellcome Trust Sanger Institute.
- ↑ "Haematology data for Crlf3". Wellcome Trust Sanger Institute.
- ↑ "Salmonella infection data for Crlf3". Wellcome Trust Sanger Institute.
- ↑ "Citrobacter infection data for Crlf3". Wellcome Trust Sanger Institute.
- 1 2 3 Gerdin AK (2010). "The Sanger Mouse Genetics Programme: High throughput characterisation of knockout mice". Acta Ophthalmologica. 88 (S248). doi:10.1111/j.1755-3768.2010.4142.x.
- ↑ Mouse Resources Portal, Wellcome Trust Sanger Institute.
- ↑ "International Knockout Mouse Consortium".
- ↑ "Mouse Genome Informatics".
- ↑ 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. - ↑ Dolgin E (June 2011). "Mouse library set to be knockout". Nature. 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718.
- ↑ 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.
- ↑ 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.
Further reading
- Visser R, Koelma N, Vijfhuizen L, et al. (2009). "RNF135 mutations are not present in patients with Sotos syndrome-like features.". Am. J. Med. Genet. A. 149A (4): 806–8. doi:10.1002/ajmg.a.32694. PMID 19291764.
- Gudbjartsson DF, Walters GB, Thorleifsson G, et al. (2008). "Many sequence variants affecting diversity of adult human height.". Nat. Genet. 40 (5): 609–15. doi:10.1038/ng.122. PMID 18391951.
- Zhao J, Li M, Bradfield JP, et al. (2010). "The role of height-associated loci identified in genome wide association studies in the determination of pediatric stature.". BMC Med. Genet. 11: 96. doi:10.1186/1471-2350-11-96. PMC 2894790. PMID 20546612.
- Yang F, Xu YP, Li J, et al. (2009). "Cloning and characterization of a novel intracellular protein p48.2 that negatively regulates cell cycle progression.". Int. J. Biochem. Cell Biol. 41 (11): 2240–50. doi:10.1016/j.biocel.2009.04.022. PMID 19427400.
- Gevaert K, Goethals M, Martens L, et al. (2003). "Exploring proteomes and analyzing protein processing by mass spectrometric identification of sorted N-terminal peptides.". Nat. Biotechnol. 21 (5): 566–9. doi:10.1038/nbt810. PMID 12665801.
- Johnatty SE, Beesley J, Chen X, et al. (2010). "Evaluation of candidate stromal epithelial cross-talk genes identifies association between risk of serous ovarian cancer and TERT, a cancer susceptibility "hot-spot".". PLoS Genet. 6 (7): e1001016. doi:10.1371/journal.pgen.1001016. PMC 2900295. PMID 20628624.
- Barbe L, Lundberg E, Oksvold P, et al. (2008). "Toward a confocal subcellular atlas of the human proteome.". Mol. Cell Proteomics. 7 (3): 499–508. doi:10.1074/mcp.M700325-MCP200. PMID 18029348.
- Douglas J, Cilliers D, Coleman K, et al. (2007). "Mutations in RNF135, a gene within the NF1 microdeletion region, cause phenotypic abnormalities including overgrowth.". Nat. Genet. 39 (8): 963–5. doi:10.1038/ng2083. PMID 17632510.