Highly specific for ethanolamine phosphorylation. Does not have choline kinase activity. ATP + ethanolamine = ADP + H(+) + phosphoethanolamine Phospholipid metabolism; phosphatidylethanolamine biosynthesis; phosphatidylethanolamine from ethanolamine: step 1/3. Expressed in testis and liver. Low expression in ovary and kidney. The expression is restricted to the gonads during the sex determination period and throughout embryogenesis. In developing testis, the expression is found only in the Sertoli cells. The expression is strongest at day 11.5, more intense in the testis than the ovary. From 12.5 dpc the expression in the ovary is reduced and disappears. The expression at day 13.5 dpc is restricted to the testis cords. No visible phenotype in adults. No significant effect is seen on liver phospholipid metabolism, neural development, or testicular function. No abnormalities are detected in embryonic and adult testis morphology, differentiation, function, or fertility. PubMed:16861741 shows maternal-specific failure to support late embryonic development, resulting in reduced perinatal size and survival and suggesting compromised placental function. Belongs to the choline/ethanolamine kinase family. According to PubMed:16861741, disruption of the gene causes increased prevalence of placental thrombosis, reduced litter size and increased pup mortality. No such effect was observed by PubMed:18755794. One possible explanation lies in the fact that PubMed:16861741 observed a remarkable 100% survival of control pups and 16% mortality for mutant pups, while PubMed:18755794 observed 16% mortality for both wild-type and mutant pups. According to PubMed:18755794, the construct used in PubMed:16861741 may lead to expression of a truncated transcript that might have deleterious effects.