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)
 

Links

 

Gene Review

Pou2af1  -  POU domain, class 2, associating factor 1

Mus musculus

Synonyms: B-cell-specific coactivator OBF-1, BOB-1, BOB.1, BOB1, Bob-1, ...
 
 
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 Pou2af1

 

High impact information on Pou2af1

  • The later identification of a membrane bound, myristoylated form of OCA-B suggested additional, unique functions in B cell signaling pathways [4].
  • This study has shown that OCA-B also functions in the pre-B1-to-pre-B2 cell transition and, most surprisingly, that it directly interacts with SYK, a tyrosine kinase critical for pre-BCR and BCR signaling [4].
  • OcaB, a transcriptional coactivator also known as Bob-1 or OBF-1, was isolated on the basis of its ability to enhance transcription of immunoglobulin (Ig) genes in vitro [5].
  • To define the in vivo role of OBF-1 we have used gene targeting in embryonic stem cells to generate mice lacking the coactivator OBF-1 [6].
  • Inducible expression and phosphorylation of coactivator BOB.1/OBF.1 in T cells [7].
 

Biological context of Pou2af1

 

Anatomical context of Pou2af1

  • Taken together, these results suggest that, at least in conventional B cells, Bob1 plays in important role in the antigen-driven stages of B cell activation and maturation [10].
  • Histological examination of sections from spleen and lymph nodes reveal that while Bob-1-deficient mice have primary follicles, they lack well-developed germinal centers [10].
  • RNAs differentially expressed in a BOB.1/OBF.1-deficient pre-B cell line and a derivative of this cell line expressing a hormone dependent BOB.1/OBF.1-estrogen receptor (BobER) fusion protein were isolated [8].
  • BOB.1/OBF.1 can efficiently activate octamer-dependent promoters in fibroblasts; however, it fails to stimulate octamer-dependent enhancer activity [11].
  • When BOB.1/OBF.1-deficient mice were crossed with Bcl2-transgenic mice, B cell development in the bone marrow and numbers of B cells in peripheral lymphoid organs were normalized [12].
 

Associations of Pou2af1 with chemical compounds

  • Induction of pre-B cells with lipopolysaccharide led to increased Oct2 levels but did not significantly increase octamer-dependent transcription in BOB.1 / OBF.1-deficient B cells [13].
  • In search of BOB.1/OBF.1 regulated genes we identified Btk--a cytoplasmic tyrosine kinase-as a direct target of BOB.1/OBF [14].
  • We show that BOB.1/OBF.1(-/-) B cells were incapable to induce BCR-triggered Ca(2+) mobilization [15].
  • Intracellular calcium (Ca2+i) was mobilized in the control cell lines but not in the OBF-1 and Vav1-deficient cells, while Xid B cell lines (btk mutant) showed a reduced Ca2+ mobilization [16].
 

Physical interactions of Pou2af1

  • These results indicate that Oct-2 and OCA-B interact with the 3' enhancer in regulation of the IgH locus during B cell activation [17].
 

Regulatory relationships of Pou2af1

  • Myosin light chain 1 atrial isoform (MLC1A) is expressed in pre-B cells under control of the BOB.1/OBF.1 coactivator [8].
  • These findings support the notion that Oct-2 regulates gene transcription by both OBF-1-dependent and -independent mechanisms [18].
  • Under these conditions, the loss of OBF-1 blocks the genetic program of ASC differentiation so that Blimp-1/prdm1 induction fails, and bcl-6, Pax5, and AID are not repressed as in control ASC [19].
 

Other interactions of Pou2af1

  • Consistent with this conclusion is the observation that transcriptional induction of the endogenous MLC1A gene by BOB.1/OBF.1 requires de novo protein synthesis [8].
  • Probably as a consequence of this reduction in mature B cells, Bob1-deficient mice show reduced serum titers of the immunoglobulin isotypes IgG1, IgG2a, IgG2b and IgA, but not IgM [10].
  • These results suggest that NFKB1 and OCA-B play compensatory roles in multiple aspects of B cell differentiation [20].
  • Oct-2 regulates CD36 gene expression via a consensus octamer, which excludes the co-activator OBF-1 [18].
  • 1. Btk, like BOB.1/OBF.1, plays a critical role in B cell development and B cell receptor signalling [14].
 

Analytical, diagnostic and therapeutic context of Pou2af1

References

  1. Up-regulation of BOB.1/OBF.1 expression in normal germinal center B cells and germinal center-derived lymphomas. Greiner, A., Müller, K.B., Hess, J., Pfeffer, K., Müller-Hermelink, H.K., Wirth, T. Am. J. Pathol. (2000) [Pubmed]
  2. Cutting edge: lack of peripheral B cells and severe agammaglobulinemia in mice simultaneously lacking Bruton's tyrosine kinase and the B cell-specific transcriptional coactivator OBF-1. Schubart, D.B., Rolink, A., Schubart, K., Matthias, P. J. Immunol. (2000) [Pubmed]
  3. Oct-2 and Bob-1 deficiency in Hodgkin and Reed Sternberg cells. Re, D., Müschen, M., Ahmadi, T., Wickenhauser, C., Staratschek-Jox, A., Holtick, U., Diehl, V., Wolf, J. Cancer Res. (2001) [Pubmed]
  4. Nontranscriptional regulation of SYK by the coactivator OCA-B is required at multiple stages of B cell development. Siegel, R., Kim, U., Patke, A., Yu, X., Ren, X., Tarakhovsky, A., Roeder, R.G. Cell (2006) [Pubmed]
  5. OcaB is required for normal transcription and V(D)J recombination of a subset of immunoglobulin kappa genes. Casellas, R., Jankovic, M., Meyer, G., Gazumyan, A., Luo, Y., Roeder, R., Nussenzweig, M. Cell (2002) [Pubmed]
  6. B-cell-specific coactivator OBF-1/OCA-B/Bob1 required for immune response and germinal centre formation. Schubart, D.B., Rolink, A., Kosco-Vilbois, M.H., Botteri, F., Matthias, P. Nature (1996) [Pubmed]
  7. Inducible expression and phosphorylation of coactivator BOB.1/OBF.1 in T cells. Zwilling, S., Dieckmann, A., Pfisterer, P., Angel, P., Wirth, T. Science (1997) [Pubmed]
  8. Myosin light chain 1 atrial isoform (MLC1A) is expressed in pre-B cells under control of the BOB.1/OBF.1 coactivator. Laumen, H., Brunner, C., Greiner, A., Wirth, T. Nucleic Acids Res. (2004) [Pubmed]
  9. The B lymphocyte-specific coactivator BOB.1/OBF.1 is required at multiple stages of B-cell development. Hess, J., Nielsen, P.J., Fischer, K.D., Bujard, H., Wirth, T. Mol. Cell. Biol. (2001) [Pubmed]
  10. B lymphocytes are impaired in mice lacking the transcriptional co-activator Bob1/OCA-B/OBF1. Nielsen, P.J., Georgiev, O., Lorenz, B., Schaffner, W. Eur. J. Immunol. (1996) [Pubmed]
  11. Functional characterization of the murine homolog of the B cell-specific coactivator BOB.1/OBF.1. Pfisterer, P., Zwilling, S., Hess, J., Wirth, T. J. Biol. Chem. (1995) [Pubmed]
  12. B cell-specific transgenic expression of Bcl2 rescues early B lymphopoiesis but not B cell responses in BOB.1/OBF.1-deficient mice. Brunner, C., Marinkovic, D., Klein, J., Samardzic, T., Nitschke, L., Wirth, T. J. Exp. Med. (2003) [Pubmed]
  13. The BOB.1 / OBF.1 co-activator is essential for octamer-dependent transcription in B cells. Laumen, H., Nielsen, P.J., Wirth, T. Eur. J. Immunol. (2000) [Pubmed]
  14. Btk expression is controlled by Oct and BOB.1/OBF.1. Brunner, C., Wirth, T. Nucleic Acids Res. (2006) [Pubmed]
  15. CD22 regulates early B cell development in BOB.1/OBF.1-deficient mice. Samardzic, T., Gerlach, J., Muller, K., Marinkovic, D., Hess, J., Nitschke, L., Wirth, T. Eur. J. Immunol. (2002) [Pubmed]
  16. Knockout B lymphoma cell lines as biochemical tools to explore multiple signalling pathways. Veale, M.F., Dietrich, W.M., Corcoran, L.M. Immunol. Cell Biol. (2003) [Pubmed]
  17. Transcriptional regulation of the murine 3' IgH enhancer by OCT-2. Tang, H., Sharp, P.A. Immunity (1999) [Pubmed]
  18. Oct-2 regulates CD36 gene expression via a consensus octamer, which excludes the co-activator OBF-1. Shore, P., Dietrich, W., Corcoran, L.M. Nucleic Acids Res. (2002) [Pubmed]
  19. Differential requirement for OBF-1 during antibody-secreting cell differentiation. Corcoran, L.M., Hasbold, J., Dietrich, W., Hawkins, E., Kallies, A., Nutt, S.L., Tarlinton, D.M., Matthias, P., Hodgkin, P.D. J. Exp. Med. (2005) [Pubmed]
  20. Genetic analyses of NFKB1 and OCA-B function: defects in B cells, serum IgM level, and antibody responses in Nfkb1-/-Oca-b-/- mice. Kim, U., Gunther, C.S., Roeder, R.G. J. Immunol. (2000) [Pubmed]
  21. Expression of the aldehyde dehydrogenase 2-like gene is controlled by BOB.1/OBF.1 in B lymphocytes. Brunner, C., Laumen, H., Nielsen, P.J., Kraut, N., Wirth, T. J. Biol. Chem. (2003) [Pubmed]
  22. The B-cell-specific transcription coactivator OCA-B/OBF-1/Bob-1 is essential for normal production of immunoglobulin isotypes. Kim, U., Qin, X.F., Gong, S., Stevens, S., Luo, Y., Nussenzweig, M., Roeder, R.G. Nature (1996) [Pubmed]
  23. Identification of transcription coactivator OCA-B-dependent genes involved in antigen-dependent B cell differentiation by cDNA array analyses. Kim, U., Siegel, R., Ren, X., Gunther, C.S., Gaasterland, T., Roeder, R.G. Proc. Natl. Acad. Sci. U.S.A. (2003) [Pubmed]
  24. The Ets factor Spi-B is a direct critical target of the coactivator OBF-1. Bartholdy, B., Du Roure, C., Bordon, A., Emslie, D., Corcoran, L.M., Matthias, P. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
 
WikiGenes - Universities