The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)



Gene Review

Pcyt1a  -  phosphate cytidylyltransferase 1, choline,...

Mus musculus

Synonyms: CCT A, CCT-alpha, CT A, CTP:phosphocholine cytidylyltransferase A, CTP:phosphocholine cytidylyltransferase alpha, ...
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of Pcyt1a

  • The 17 monoclonal antibodies were divided into a minimum of seven different specificity groups based on their abilities to bind to the following purified test antigens in solid-phase radioimmunoassays: CT, the A and B polypeptides of CT (CT-A and CT-B, respectively), and the heat-labile enterotoxins designated LTh and LTp from Escherichia coli [1].

High impact information on Pcyt1a


Biological context of Pcyt1a

  • After synchronizing the cell cycle in NIH3T3 cells, CTalpha mRNA increased at the S-M phase corresponding to an increase of Ets-1 mRNA and a decrease of Net mRNA [4].
  • RNA interference targeting Net caused an increase of endogenous CTalpha mRNA [4].
  • Previous studies (Golfman, L. S., Bakovic, M., and Vance, D. E. (2001) J. Biol. Chem. 276, 43688-43692) demonstrated that CT alpha mRNA accumulates during S phase in preparation for cellular mitosis [5].
  • These results enhance our understanding of the regulatory mechanisms involved in the expression of CTalpha in preparation for cell division [6].
  • Transcriptional enhancer factor-4 (TEF-4) enhances the transcription of CTalpha in COS-7 cells by interactions with the basal transcription machinery (Sugimoto, H., Bakovic, M., Yamashita, S., and Vance, D.E. (2001) J. Biol. Chem. 276,12338-12344) [7].

Anatomical context of Pcyt1a


Associations of Pcyt1a with chemical compounds


Physical interactions of Pcyt1a

  • Previously, we identified an Ets-1-binding site located at -49/-47 in the promoter of Pcyt1a as an important transcriptional element involved in basal CTalpha transcription (Sugimoto, H., Sugimoto, S., Tatei, K., Obinata, H., Bakovic, M., Izumi, T., and Vance, D. E. (2003) J. Biol. Chem. 278, 19716-19722) [4].
  • We conclude that Sp1 binding to the CT alpha proximal promoter is necessary to enhance transcription during the S phase [5].

Enzymatic interactions of Pcyt1a


Regulatory relationships of Pcyt1a


Other interactions of Pcyt1a


Analytical, diagnostic and therapeutic context of Pcyt1a

  • A genomic clone was isolated and the chromosomal location of the Ctpct locus determined by Southern blot hybridization of DNAs from a panel of interspecific backcross progeny derived from matings of [(C57BL/6J x Mus spretus)F1 x C57BL/6J] mice [16].
  • Indirect immunofluorescence of these cells with anti-CCT alpha antibodies resulted in a similar distribution [10].
  • The toxin analogs reacted with antibodies against CT-A and CT-B on cellulose acetate strips and in a GM1 enzyme-linked immunosorbent assay; they reacted appropriately with B-subunit epitype-specific monoclonal antibodies in checkerboard immunoblots, and they formed precipitin bands with GM1-ganglioside in Ouchterlony tests [17].
  • By means of site-directed mutagenesis, an analog of the CT-A subunit gene was created with codon substitutions for both Arg-7 and Glu-112, each of which has been shown to produce subunits lacking ADP-ribosyltransferase activity [17].
  • The binding of these antibodies to the following subunits and fragments of CT was also determined in Western blots: pentameric CT-B, monomeric CT-B, intact CT-A, and the A1 fragment of CT-A [1].


  1. Characterization of monoclonal antibodies that react with unique and cross-reacting determinants of cholera enterotoxin and its subunits. Holmes, R.K., Twiddy, E.M. Infect. Immun. (1983) [Pubmed]
  2. Early embryonic lethality in mice with targeted deletion of the CTP:phosphocholine cytidylyltransferase alpha gene (Pcyt1a). Wang, L., Magdaleno, S., Tabas, I., Jackowski, S. Mol. Cell. Biol. (2005) [Pubmed]
  3. Caspase processing and nuclear export of CTP:phosphocholine cytidylyltransferase alpha during farnesol-induced apoptosis. Lagace, T.A., Miller, J.R., Ridgway, N.D. Mol. Cell. Biol. (2002) [Pubmed]
  4. Sp1 is a co-activator with Ets-1, and Net is an important repressor of the transcription of CTP:phosphocholine cytidylyltransferase alpha. Sugimoto, H., Okamura, K., Sugimoto, S., Satou, M., Hattori, T., Vance, D.E., Izumi, T. J. Biol. Chem. (2005) [Pubmed]
  5. Activation of CTP:phosphocholine cytidylyltransferase alpha expression during the S phase of the cell cycle is mediated by the transcription factor Sp1. Banchio, C., Schang, L.M., Vance, D.E. J. Biol. Chem. (2003) [Pubmed]
  6. Phosphorylation of Sp1 by cyclin-dependent kinase 2 modulates the role of Sp1 in CTP:phosphocholine cytidylyltransferase alpha regulation during the S phase of the cell cycle. Banchio, C., Schang, L.M., Vance, D.E. J. Biol. Chem. (2004) [Pubmed]
  7. Identification of Ets-1 as an important transcriptional activator of CTP:phosphocholine cytidylyltransferase alpha in COS-7 cells and co-activation with transcriptional enhancer factor-4. Sugimoto, H., Sugimoto, S., Tatei, K., Obinata, H., Bakovic, M., Izumi, T., Vance, D.E. J. Biol. Chem. (2003) [Pubmed]
  8. Macrophages deficient in CTP:Phosphocholine cytidylyltransferase-alpha are viable under normal culture conditions but are highly susceptible to free cholesterol-induced death. Molecular genetic evidence that the induction of phosphatidylcholine biosynthesis in free cholesterol-loaded macrophages is an adaptive response. Zhang, D., Tang, W., Yao, P.M., Yang, C., Xie, B., Jackowski, S., Tabas, I. J. Biol. Chem. (2000) [Pubmed]
  9. Role of histone deacetylase in the expression of CTP:phosphocholine cytidylyltransferase alpha. Banchio, C., Lingrell, S., Vance, D.E. J. Biol. Chem. (2006) [Pubmed]
  10. CTP:phosphocholine cytidylyltransferase alpha is a cytosolic protein in pulmonary epithelial cells and tissues. Ridsdale, R., Tseu, I., Wang, J., Post, M. J. Biol. Chem. (2001) [Pubmed]
  11. Physiological regulation of phospholipid methylation alters plasma homocysteine in mice. Jacobs, R.L., Stead, L.M., Devlin, C., Tabas, I., Brosnan, M.E., Brosnan, J.T., Vance, D.E. J. Biol. Chem. (2005) [Pubmed]
  12. Targeted deletion of hepatic CTP:phosphocholine cytidylyltransferase alpha in mice decreases plasma high density and very low density lipoproteins. Jacobs, R.L., Devlin, C., Tabas, I., Vance, D.E. J. Biol. Chem. (2004) [Pubmed]
  13. Hepatic CTP:phosphocholine cytidylyltransferase-alpha is a critical predictor of plasma high density lipoprotein and very low density lipoprotein. Jacobs, R.L., Lingrell, S., Zhao, Y., Francis, G.A., Vance, D.E. J. Biol. Chem. (2008) [Pubmed]
  14. Functional significance of Sp1, Sp2, and Sp3 transcription factors in regulation of the murine CTP:phosphocholine cytidylyltransferase alpha promoter. Bakovic, M., Waite, K.A., Vance, D.E. J. Lipid Res. (2000) [Pubmed]
  15. Surfactant lipid synthesis and lamellar body formation in glycogen-laden type II cells. Ridsdale, R., Post, M. Am. J. Physiol. Lung Cell Mol. Physiol. (2004) [Pubmed]
  16. The gene for murine CTP:phosphocholine cytidylyltransferase (Ctpct) is located on mouse chromosome 16. Rutherford, M.S., Rock, C.O., Jenkins, N.A., Gilbert, D.J., Tessner, T.G., Copeland, N.G., Jackowski, S. Genomics (1993) [Pubmed]
  17. Construction and characterization of recombinant Vibrio cholerae strains producing inactive cholera toxin analogs. Häse, C.C., Thai, L.S., Boesman-Finkelstein, M., Mar, V.L., Burnette, W.N., Kaslow, H.R., Stevens, L.A., Moss, J., Finkelstein, R.A. Infect. Immun. (1994) [Pubmed]
WikiGenes - Universities