磷酸乙醇胺转移酶A抗体说明书

磷酸乙醇胺转移酶A抗体说明书Background: Increase in fetal surfactant synthesis and lung maturity is caused by the glucocorticoidal induction of enzymes required for phosphatidylcholine synthesis towards the end of gestation (1). The regulation of gestational age-dependent induction of phosphatidylcholine synthesis by glucocorticoids is still unclear (1). The rate-controlling enzyme in the phosphatidylcholine biosynthetic pathway is CTP-phosphocholine cytidylyltransferase A (CCT A) (2–4). In cultured eukaryotic cells, this enzyme is essential for survival (3). The alpha isoform is located in the nucleus and is regulated by reversible phosphorylation and membrane association (3). There is significant identity between the alpha-helical membrane-binding domains of CCT A and soybean oleosin (2). Expressed CCT A has lipid-dependent cytidylyltransferase activity (5). The gene which encodes CCT A maps to human chromosome 3q (4). Also known as: CCT A; CCT alpha; CCT-alpha; Choline phosphate cytidylyltransferase A; Choline-phosphate cytidylyltransferase A; CT A; CT antibody CTP:phosphocholine cytidylyltransferase A; CTPCT; PCY1A_HUMAN; PCYT1; Pcyt1a; Phosphate cytidylyltransferase 1 choline alpha; Phosphate cytidylyltransferase 1 choline alpha isoform; Phosphorylcholine transferase A.磷酸乙醇胺转移酶A抗体说明书