Model organisms have been used in the study of CRLF3 function. A conditional knockout mouse line, called Crlf3tm1a(KOMP)Wtsi[12][13] 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.[14][15][16] Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.[10][17] Twenty six tests were carried out and two significant phenotypes were reported. Homozygousmutant female adults had a significant increase in circulating levels of fructosamine, while mutants of both sexes had decreased platelet cell numbers.[10]
Function[]
Although CRLF3 signaling pathways have not yet been fully characterized it is very likely that CRLF3 is a neuroprotective erythropoietin receptor.[18]
Origin[]
Phylogenetic analyses have shown that CRLF3 at first appeared in a common ancestor of Cnidaria and Bilateria and hence emerged with the origin of the nervous system.[19][20]
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