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Gene Review

BTK  -  Bruton agammaglobulinemia tyrosine kinase

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Disease relevance of BTK

  • Here, we report that the calcium ionophore ionomycin induces a massive Ca2+-dependent apoptosis in wildtype DT-40 chicken B lymphoma cells, as well as in BTK-deficient, PLCgamma2-deficient and IP3 receptor-deficient DT-40 cells, but not in LYN- or SYK-deficient DT-40 cells [1].
  • Defects in the gene encoding Bruton's tyrosine kinase (Btk) result in a disease called X-linked agammaglobulinemia, in which there is a profound decrease of mature B cells due to a block in B cell development [2].

High impact information on BTK

  • A role for Bruton's tyrosine kinase in B cell antigen receptor-mediated activation of phospholipase C-gamma 2 [2].
  • Bruton's tyrosine kinase deficiency in macrophages inhibits nitric oxide generation leading to enhancement of IL-12 induction [3].
  • Here, we provide experimental evidence that the cytoplasmic tyrosine kinases BTK, SYK, and LYN are not required for this signal [4].
  • Not only Lyn, but also Syk was required for tyrosine phosphorylation of Btk in BCR signaling [5].
  • Cross-linking of BCR induces phosphorylation of Btk at Tyr551 and Tyr223 [5].

Biological context of BTK

  • These BTK-deficient cells were highly resistant to oxidative stress-induced apoptosis triggered by PV treatment [6].
  • BTK physically associated with and tyrosine phosphorylated STAT3; this association was promoted by pervanadate (PV)-induced oxidative stress [6].
  • We discovered that Bruton's tyrosine kinase (BTK) and phospholipase C-gamma2 (PLC-gamma2) are required to activate NFAT and NF-kappaB, and to produce the lipid second messenger diacylglycerol in response to BCR cross-linking [7].
  • Employing chimeric Btk with green fluorescent protein in transient transfections resulted in Btk translocation to the cytoplasmic membrane of live cells through various forms of upstream PI 3-K activation [8].

Anatomical context of BTK

  • Defective BTK expression in leukaemic B-cell precursors from infants with t(4;11) acute lymphoblastic leukaemia has been associated with radiation resistance [6].
  • A gain-of-function mutant of Btk was found to be a potent inducer of lamellipodia and/or membrane ruffle formation [8].

Analytical, diagnostic and therapeutic context of BTK


  1. SYK and LYN mediate B-cell receptor-independent calcium-induced apoptosis in DT-40 lymphoma B-cells. Zhu, D.M., Tibbles, H.E., Vassilev, A.O., Uckun, F.M. Leuk. Lymphoma (2002) [Pubmed]
  2. A role for Bruton's tyrosine kinase in B cell antigen receptor-mediated activation of phospholipase C-gamma 2. Takata, M., Kurosaki, T. J. Exp. Med. (1996) [Pubmed]
  3. Bruton's tyrosine kinase deficiency in macrophages inhibits nitric oxide generation leading to enhancement of IL-12 induction. Mukhopadhyay, S., George, A., Bal, V., Ravindran, B., Rath, S. J. Immunol. (1999) [Pubmed]
  4. Role of tyrosine kinases in induction of the c-jun proto-oncogene in irradiated B-lineage lymphoid cells. Goodman, P.A., Niehoff, L.B., Uckun, F.M. J. Biol. Chem. (1998) [Pubmed]
  5. Transphosphorylation of Bruton's tyrosine kinase on tyrosine 551 is critical for B cell antigen receptor function. Kurosaki, T., Kurosaki, M. J. Biol. Chem. (1997) [Pubmed]
  6. Bruton's tyrosine kinase prevents activation of the anti-apoptotic transcription factor STAT3 and promotes apoptosis in neoplastic B-cells and B-cell precursors exposed to oxidative stress. Uckun, F., Ozer, Z., Vassilev, A. Br. J. Haematol. (2007) [Pubmed]
  7. B-cell antigen receptor activates transcription factors NFAT (nuclear factor of activated T-cells) and NF-kappaB (nuclear factor kappaB) via a mechanism that involves diacylglycerol. Antony, P., Petro, J.B., Carlesso, G., Shinners, N.P., Lowe, J., Khan, W.N. Biochem. Soc. Trans. (2004) [Pubmed]
  8. Redistribution of Bruton's tyrosine kinase by activation of phosphatidylinositol 3-kinase and Rho-family GTPases. Nore, B.F., Vargas, L., Mohamed, A.J., Brandén, L.J., Bäckesjö, C.M., Islam, T.C., Mattsson, P.T., Hultenby, K., Christensson, B., Smith, C.I. Eur. J. Immunol. (2000) [Pubmed]
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