CRLF3

Cytokine receptor-like factor 3
Identifiers
Symbols	CRLF3 ; CREME-9; CREME9; CRLM9; CYTOR4; FRWS; p48.2
External IDs	OMIM: 614853 HomoloGene: 9327 GeneCards: CRLF3 Gene
Gene ontology Molecular function • protein binding Cellular component • cytoplasm • plasma membrane Biological process • G1/S transition of mitotic cell cycle • negative regulation of cell growth • positive regulation of transcription, DNA-templated • positive regulation of transcription from RNA polymerase II promoter • positive regulation of JAK-STAT cascade • positive regulation of cell cycle arrest Sources: Amigo / QuickGO
Orthologs
Species	Human	Mouse
Entrez	51379	54394
Ensembl	ENSG00000176390	ENSMUSG00000017561
UniProt	Q8IUI8	Q9Z2L7
RefSeq (mRNA)	NM_015986	NM_001277106
RefSeq (protein)	NP_057070	NP_001264035
Location (UCSC)	Chr 17: 30.77 – 30.82 Mb	Chr 11: 80.05 – 80.08 Mb
PubMed search

Cytokine receptor-like factor 3 is a protein that in humans is encoded by the CRLF3 gene.^[1]

Model organisms

Crlf3 knockout mouse phenotype

Characteristic	Phenotype
Homozygote viability	Normal
Fertility	Normal
Body weight	Normal
Anxiety	Normal
Neurological assessment	Normal
Grip strength	Normal
Hot plate	Normal
Dysmorphology	Normal
Indirect calorimetry	Normal
Glucose tolerance test	Normal
Auditory brainstem response	Normal
DEXA	Normal
Radiography	Normal
Body temperature	Normal
Eye morphology	Normal
Clinical chemistry	Abnormal[2]
Plasma immunoglobulins	Normal
Haematology	Abnormal[3]
Peripheral blood lymphocytes	Normal
Micronucleus test	Normal
Heart weight	Normal
Tail epidermis wholemount	Normal
Skin Histopathology	Normal
Brain histopathology	Normal
Salmonella infection	Normal[4]
Citrobacter infection	Normal[5]
All tests and analysis from[6][7]

Model organisms have been used in the study of CRLF3 function. A conditional knockout mouse line, called Crlf3^{tm1a(KOMP)Wtsi[8][9]} 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.^[10][11][12] Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.^[6][13] 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.^[6]

References

1. "Entrez Gene: cytokine receptor-like factor 3".
2. "Clinical chemistry data for Crlf3". Wellcome Trust Sanger Institute.
3. "Haematology data for Crlf3". Wellcome Trust Sanger Institute.
4. "Salmonella infection data for Crlf3". Wellcome Trust Sanger Institute.
5. "Citrobacter infection data for Crlf3". Wellcome Trust Sanger Institute.
6. 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.
7. Mouse Resources Portal, Wellcome Trust Sanger Institute.
8. "International Knockout Mouse Consortium".
9. "Mouse Genome Informatics".
10. 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.
11. Dolgin E (June 2011). "Mouse library set to be knockout". Nature 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718.
12. 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.
13. 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.