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. The regulation of gestational age-dependent induction of phosphatidylcholine synthesis by glucocorticoids is still unclear. The rate-controlling enzyme in the phosphatidylcholine biosynthetic pathway is CTP-phosphocholine cytidylyltransferase A (CCT A). 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. There is significant identity between the alpha-helical membrane-binding domains of CCT A and soybean oleosin. Expressed CCT A has lipid-dependent cytidylyltransferase activity (5). The gene which encodes CCT A maps to human chromosome 3q.

Description: Rabbit polyclonal to PCYT1A

Immunogen: KLH conjugated synthetic peptide derived from PCYT1A

Specificity:  ·Reacts with Human, Mouse and Rat.

·Isotype: IgG

Application:  ·Western blotting: 1/100-500. Predicted Mol wt: 42 kDa;

·Immunohistochemistry (Paraffin/frozen tissue section): 1/50-200;

·Immunocytochemistry/Immunofluorescence: 1/100;

·Immunoprecipitation: 1/50;

·ELISA: 1/500;

·Optimal working dilutions must be determined by the end user.