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Blnk  -  B cell linker

Mus musculus

Synonyms: B-cell adapter containing a SH2 domain protein, B-cell adapter containing a Src homology 2 domain protein, B-cell linker protein, BASH, BCA, ...
 
 
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Disease relevance of Blnk

  • Our recent findings of defective SLP-65 expression in approximately 50% of childhood pre-B acute lymphoblastic leukemias and spontaneous pre-B cell lymphoma development in SLP-65-/- mice demonstrate that SLP-65 acts as a tumor suppressor [1].
  • In the mouse, the downstream signaling molecules SLP-65 and Btk cooperate to limit proliferation and induce differentiation of pre-B cells, thereby acting as tumor suppressors to prevent pre-B cell leukemia [2].
  • To determine whether macrophages functioned normally in vivo, we infected WT and SLP-76(-/-) SLP-65(-/-) mice with sublethal doses of Listeria monocytogenes (LM), a bacterium against which the initial host defense is provided by activated macrophages [3].
  • A new tumor-associated antigen expressed on breast carcinomas, defined by monoclonal antibody BCA 227 [4].
  • All these data are in favor of the use of mAb BCA 227 as an immunodiagnostic tool for breast cancer [4].
 

High impact information on Blnk

  • B cell development in BLNK-/- mice was blocked at the transition from B220+CD43+ progenitor B to B220+CD43- precursor B cells [5].
  • In B cells, B cell linker protein (BLNK) links the B cell receptor (BCR)-activated Syk kinase to the phosphoinositide and mitogen-activated kinase pathways [5].
  • Together, our results suggest that the adaptor proteins LAT and SLP-76 are involved in pre-BCR signaling, thereby rescuing arrested murine SLP-65(-/-) pre-B cells [6].
  • Reconstitution of LAT or SLP-65 expression in SLP-65/LAT(-/-) pre-B cells restored their calcium (Ca2+) mobilization capacity, led to downregulation of surface pre-BCR, and induced differentiation to BCR+ cells [6].
  • Ig(mu)(+) Pax5(-/-) pro-B cells expressing a BLNK-estrogen receptor fusion protein initiated signaling immediately upon hormone addition, which facilitated analysis of pre-BCR-induced gene expression changes [7].
 

Chemical compound and disease context of Blnk

 

Biological context of Blnk

  • These results suggest that Igalpha non-ITAM tyrosine 204 promotes a distinct cellular response, namely T-independent B cell proliferation and differentiation via phosphorylation of the adaptor BLNK [9].
  • Restoration of BLNK expression in Ig(mu) transgenic Pax5(-/-) pro-B cells resulted in constitutive pre-BCR signaling and increased cell proliferation without inducing progression to the pre-B cell stage [7].
  • During signal transduction through the B cell antigen receptor (BCR), several signaling elements are brought together by the adaptor protein SLP-65 [10].
  • Finally, splenic B cells in BCR-transgenic BLNK(-/-) mice are predominantly of the transitional B cell phenotype and are rapidly lost from the peripheral B cell pool [11].
  • B cell linker (BLNK) protein is a component of the B cell receptor (BCR) signaling pathway and BLNK(-/-) mice have a block in B lymphopoiesis at the pro-B/pre-B cell stage [11].
 

Anatomical context of Blnk

 

Associations of Blnk with chemical compounds

  • These results show that SLP65/BLNK is not absolutely essential for Ca(2+) induction in B cells, because the deficiency of this adapter can be by-passed by the additional deletion of an inhibitory receptor [17].
  • BCA-induced apoptosis was blocked by pretreatment of cells with anti-oxidants, glutathione, or N-acetyl-cysteine [18].
  • Acetylation of BCA with acetic anhydride converts all 18 lysine-epsilon-NH(3)(+) groups to lysine-epsilon-NHCOCH(3) groups and generates BCA-Ac(18) [19].
  • This study compares the folding of two polypeptides--bovine carbonic anhydrase (BCA) and peracetylated BCA (BCA-Ac(18))--having the same sequence of amino acids but differing by 18 formal units of charge, from a solution containing denaturing concentrations of sodium dodecyl sulfate (SDS) [19].
  • Regulation of BLNK recruitment was dependent upon the Grap2 proline-rich domain, while modulation of phosphorylation was dependent upon both the proline-rich and SH2 domains [20].
 

Regulatory relationships of Blnk

 

Other interactions of Blnk

 

Analytical, diagnostic and therapeutic context of Blnk

References

  1. Bruton's tyrosine kinase cooperates with the B cell linker protein SLP-65 as a tumor suppressor in Pre-B cells. Kersseboom, R., Middendorp, S., Dingjan, G.M., Dahlenborg, K., Reth, M., Jumaa, H., Hendriks, R.W. J. Exp. Med. (2003) [Pubmed]
  2. Involvement of SLP-65 and Btk in tumor suppression and malignant transformation of pre-B cells. Hendriks, R.W., Kersseboom, R. Semin. Immunol. (2006) [Pubmed]
  3. Macrophage activation and Fcgamma receptor-mediated signaling do not require expression of the SLP-76 and SLP-65 adaptors. Nichols, K.E., Haines, K., Myung, P.S., Newbrough, S., Myers, E., Jumaa, H., Shedlock, D.J., Shen, H., Koretzky, G.A. J. Leukoc. Biol. (2004) [Pubmed]
  4. A new tumor-associated antigen expressed on breast carcinomas, defined by monoclonal antibody BCA 227. Blottière, H.M., Pelhate, S., Aubry, J., Kremer, M., Thedrez, P., Sai-Maurel, C., Douillard, J.Y., Chatal, J.F. Cancer Res. (1991) [Pubmed]
  5. Requirement for B cell linker protein (BLNK) in B cell development. Pappu, R., Cheng, A.M., Li, B., Gong, Q., Chiu, C., Griffin, N., White, M., Sleckman, B.P., Chan, A.C. Science (1999) [Pubmed]
  6. LAT links the pre-BCR to calcium signaling. Su, Y.W., Jumaa, H. Immunity (2003) [Pubmed]
  7. Control of pre-BCR signaling by Pax5-dependent activation of the BLNK gene. Schebesta, M., Pfeffer, P.L., Busslinger, M. Immunity (2002) [Pubmed]
  8. Delayed occurrence of H-ras12V-induced hepatocellular carcinoma with long-term treatment with cinnamaldehydes. Moon, E.Y., Lee, M.R., Wang, A.G., Lee, J.H., Kim, H.C., Kim, H.M., Kim, J.M., Kwon, B.M., Yu, D.Y. Eur. J. Pharmacol. (2006) [Pubmed]
  9. The B cell receptor promotes B cell activation and proliferation through a non-ITAM tyrosine in the Igalpha cytoplasmic domain. Patterson, H.C., Kraus, M., Kim, Y.M., Ploegh, H., Rajewsky, K. Immunity (2006) [Pubmed]
  10. Abnormal development and function of B lymphocytes in mice deficient for the signaling adaptor protein SLP-65. Jumaa, H., Wollscheid, B., Mitterer, M., Wienands, J., Reth, M., Nielsen, P.J. Immunity (1999) [Pubmed]
  11. Delayed cellular maturation and decreased immunoglobulin kappa light chain production in immature B lymphocytes lacking B cell linker protein. Xu, S., Lam, K.P. J. Exp. Med. (2002) [Pubmed]
  12. Immune functions in mice lacking Clnk, an SLP-76-related adaptor expressed in a subset of immune cells. Utting, O., Sedgmen, B.J., Watts, T.H., Shi, X., Rottapel, R., Iulianella, A., Lohnes, D., Veillette, A. Mol. Cell. Biol. (2004) [Pubmed]
  13. R406, an orally available spleen tyrosine kinase inhibitor blocks fc receptor signaling and reduces immune complex-mediated inflammation. Braselmann, S., Taylor, V., Zhao, H., Wang, S., Sylvain, C., Baluom, M., Qu, K., Herlaar, E., Lau, A., Young, C., Wong, B.R., Lovell, S., Sun, T., Park, G., Argade, A., Jurcevic, S., Pine, P., Singh, R., Grossbard, E.B., Payan, D.G., Masuda, E.S. J. Pharmacol. Exp. Ther. (2006) [Pubmed]
  14. Adapter proteins SLP-76 and BLNK both are expressed by murine macrophages and are linked to signaling via Fcgamma receptors I and II/III. Bonilla, F.A., Fujita, R.M., Pivniouk, V.I., Chan, A.C., Geha, R.S. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  15. The absence of SLP65 and Btk blocks B cell development at the preB cell receptor-positive stage. Jumaa, H., Mitterer, M., Reth, M., Nielsen, P.J. Eur. J. Immunol. (2001) [Pubmed]
  16. Tumor suppressor function of Bruton tyrosine kinase is independent of its catalytic activity. Middendorp, S., Zijlstra, A.J., Kersseboom, R., Dingjan, G.M., Jumaa, H., Hendriks, R.W. Blood (2005) [Pubmed]
  17. B cell defects in SLP65/BLNK-deficient mice can be partially corrected by the absence of CD22, an inhibitory coreceptor for BCR signaling. Gerlach, J., Ghosh, S., Jumaa, H., Reth, M., Wienands, J., Chan, A.C., Nitschke, L. Eur. J. Immunol. (2003) [Pubmed]
  18. 2'-benzoyloxycinnamaldehyde induces apoptosis in human carcinoma via reactive oxygen species. Han, D.C., Lee, M.Y., Shin, K.D., Jeon, S.B., Kim, J.M., Son, K.H., Kim, H.C., Kim, H.M., Kwon, B.M. J. Biol. Chem. (2004) [Pubmed]
  19. Eliminating positively charged lysine epsilon-NH3+ groups on the surface of carbonic anhydrase has no significant influence on its folding from sodium dodecyl sulfate. Gudiksen, K.L., Gitlin, I., Yang, J., Urbach, A.R., Moustakas, D.T., Whitesides, G.M. J. Am. Chem. Soc. (2005) [Pubmed]
  20. Spi-1 and Spi-B control the expression of the Grap2 gene in B cells. Garrett-Sinha, L.A., Hou, P., Wang, D., Grabiner, B., Araujo, E., Rao, S., Yun, T.J., Clark, E.A., Simon, M.C., Clark, M.R. Gene (2005) [Pubmed]
  21. Haploinsufficiency of B cell linker protein enhances B cell signaling defects in mice expressing a limiting dosage of Bruton's tyrosine kinase. Whyburn, L.R., Halcomb, K.E., Contreras, C.M., Pappu, R., Witte, O.N., Chan, A.C., Satterthwaite, A.B. Int. Immunol. (2003) [Pubmed]
  22. Differential involvement of IFN-beta in Toll-like receptor-stimulated dendritic cell activation. Hoshino, K., Kaisho, T., Iwabe, T., Takeuchi, O., Akira, S. Int. Immunol. (2002) [Pubmed]
  23. Receptor-facilitated antigen presentation requires the recruitment of B cell linker protein to Igalpha. Siemasko, K., Skaggs, B.J., Kabak, S., Williamson, E., Brown, B.K., Song, W., Clark, M.R. J. Immunol. (2002) [Pubmed]
  24. The B cell-restricted adaptor BASH is required for normal development and antigen receptor-mediated activation of B cells. Hayashi, K., Nittono, R., Okamoto, N., Tsuji, S., Hara, Y., Goitsuka, R., Kitamura, D. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  25. Characterization of the B cell-specific adaptor SLP-65 and other protein tyrosine kinase substrates by two-dimensional gel electrophoresis. Wollscheid, B., Reth, M., Wienands, J. Immunol. Lett. (1999) [Pubmed]
  26. Inhibition of human tumor growth by 2'-hydroxy- and 2'-benzoyloxycinnamaldehydes. Lee, C.W., Hong, D.H., Han, S.B., Park, S.H., Kim, H.K., Kwon, B.M., Kim, H.M. Planta Med. (1999) [Pubmed]
 
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