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Rabbit Anti-PCYT1A /FITC Conjugated antibody
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).
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 SLCterminus 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.
Database links:
Entrez Gene: 5130 Human
Entrez Gene: 13026 Mouse
Omim: 123695 Human
SwissProt: P49585 Human
SwissProt: P49586 Mouse
Unigene: 135997 Human
Unigene: 98775 Mouse
Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
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