免 疫 原：KLH conjugated synthetic peptide derived from human PCYT1A
抗原表位：201-300/367
SWISS：P49585
Gene ID ：5130
Human Gene ID：5130

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).
Function：Controls phosphatidylcholine synthesis.
Subunit：Homodimer.
Subcellular Location：Cytoplasm; cytosol. Membrane. It can interconvert between an inactive cytosolic form and an active membrane-bound form.
Post-translational modifications：The serine residues of the C-terminus are phosphorylated. The inactive soluble form is stabilized by phosphorylation, the active membrane bound form is promoted by anionic lipids or diacylglycerol, and is stabilized by dephosphorylation.
Similarity：Belongs to the cytidylyltransferase family.
Important Note：This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.