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Gene Review

Bst1  -  bone marrow stromal cell antigen 1

Mus musculus

Synonyms: 114/A10, A530073F09, ADP-ribosyl cyclase 2, ADP-ribosyl cyclase/cyclic ADP-ribose hydrolase 2, Antigen BP3, ...
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Disease relevance of Bst1

  • Strain BST-1 is a derivative of Escherichia coli K-12 that carries a plasmid designated pURA-4 and is the expression system used by The Upjohn Company in the production of recombinant bovine somatotropin (rbSt) [1].

High impact information on Bst1

  • Prader-Willi and Angelman syndromes (PWS and AS) typically result from an approximately 4-Mb deletion of human chromosome 15q11-q13, with clustered breakpoints (BP) at either of two proximal sites (BP1 and BP2) and one distal site (BP3) [2].
  • The low density of BST-1 expression on bone marrow (BM) stromal cells and the low specific activity of the enzyme made it unclear whether cADPR generation by a BST-1(+) stroma could stimulate HP proliferation in the BM microenvironment [3].
  • Concentrative uptake of cyclic ADP-ribose generated by BST-1+ stroma stimulates proliferation of human hematopoietic progenitors [3].
  • We developed and characterized two BST-1(+) stromal cell lines, expressing an ectocellular cyclase activity similar to that of BST-1(+) human mesenchymal stem cells, the precursors of BM stromal cells [3].
  • Influx of paracrinally generated cADPR into clonogenic HP was mediated by a concentrative, nitrobenzylthioinosine- and dipyridamole-inhibitable nucleoside transporter, this providing a possible explanation to the effectiveness of the hormone-like concentrations of the cyclic nucleotide measured in the medium conditioned by BST-1(+) feeders [3].

Biological context of Bst1


Anatomical context of Bst1


Associations of Bst1 with chemical compounds


Other interactions of Bst1


Analytical, diagnostic and therapeutic context of Bst1


  1. Absence of persistence and transfer of genetic material by recombinant Escherichia coli in conventional, antibiotic-treated mice. Yancey, R.J., Kotarski, S.F., Thurn, K.K., Lepley, R.A., Mott, J.E. J. Ind. Microbiol. (1993) [Pubmed]
  2. Identification of four highly conserved genes between breakpoint hotspots BP1 and BP2 of the Prader-Willi/Angelman syndromes deletion region that have undergone evolutionary transposition mediated by flanking duplicons. Chai, J.H., Locke, D.P., Greally, J.M., Knoll, J.H., Ohta, T., Dunai, J., Yavor, A., Eichler, E.E., Nicholls, R.D. Am. J. Hum. Genet. (2003) [Pubmed]
  3. Concentrative uptake of cyclic ADP-ribose generated by BST-1+ stroma stimulates proliferation of human hematopoietic progenitors. Podestà, M., Benvenuto, F., Pitto, A., Figari, O., Bacigalupo, A., Bruzzone, S., Guida, L., Franco, L., Paleari, L., Bodrato, N., Usai, C., De Flora, A., Zocchi, E. J. Biol. Chem. (2005) [Pubmed]
  4. Stage-specific expression of mouse BST-1/BP-3 on the early B and T cell progenitors prior to gene rearrangement of antigen receptor. Ishihara, K., Kobune, Y., Okuyama, Y., Itoh, M., Lee, B.O., Muraoka, O., Hirano, T. Int. Immunol. (1996) [Pubmed]
  5. The murine BP-3 gene encodes a relative of the CD38/NAD glycohydrolase family. Dong, C., Wang, J., Neame, P., Cooper, M.D. Int. Immunol. (1994) [Pubmed]
  6. Genomic organization and chromosomal localization of the mouse Bp3 gene, a member of the CD38/ADP-ribosyl cyclase family. Dong, C., Willerford, D., Alt, F.W., Cooper, M.D. Immunogenetics (1996) [Pubmed]
  7. Molecular cloning of murine BST-1 having homology with CD38 and Aplysia ADP-ribosyl cyclase. Itoh, M., Ishihara, K., Tomizawa, H., Tanaka, H., Kobune, Y., Ishikawa, J., Kaisho, T., Hirano, T. Biochem. Biophys. Res. Commun. (1994) [Pubmed]
  8. Novel kinetics, behaviour and cell-type specificity of CD157-mediated tyrosine kinase signalling. Hussain, A.M., Chang, C.F. Cell. Signal. (1999) [Pubmed]
  9. Regulation of insulin-like growth factor-I and binding protein-3 expression in oMtla-oGH transgenic mice. Chow, J.C., Murray, J.D., Pomp, D., Baldwin, R.L., Calvert, C.C., Oberbauer, A.M. Transgenic Res. (1994) [Pubmed]
  10. Transfection of human insulin-like growth factor-binding protein 3 gene inhibits cell growth and tumorigenicity: a cell culture model for lung cancer. Hochscheid, R., Jaques, G., Wegmann, B. J. Endocrinol. (2000) [Pubmed]
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