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Blood, 1 August 2006, Vol. 108, No. 3, pp. 904-907. Prepublished online as a Blood First Edition Paper on March 30, 2006; DOI 10.1182/blood-2005-12-4885. This Article Full Text (PDF) All Versions of this Article: 2005-12-4885v1 108/3/904    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Lee, B.-C. Articles by Karsenty Avraham, H. Search for Related Content PubMed PubMed Citation Articles by Lee, B.-C. Articles by Karsenty Avraham, H. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted December 13, 2005 Accepted March 23, 2006 Identification of the non-receptor tyrosine kinase MATK/CHK as an essential regulator of immune cells using Matk/CHK deficient mice Byeong-Chel Lee, Shalom Avraham, Akira Imamoto, and Hava Karsenty Avraham* Division of Experimental Medicine, Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine, Harvard Medical School, Boston, MA, USA The Ben May Institute for Cancer Research, The University of Chicago, Chicago, IL, USA * Corresponding author; email: havraham{at}bidmc.harvard.edu. Matk/CHK knockout mice were reported to show no apparent phenotypic abnormalities. This was thought to be due to the homologous kinase Csk that compensates for Matk/CHK. Here, we present the first evidence that the non-receptor tyrosine kinase, Matk/CHK, is an important modulator of immune cell signaling. We found that the frequency of primitive hematopoietic cells, the side population c-kit+ Lin- Sca-1+ (SPKLS) cells, in Matk/CHK-/- mice was increased 2.2-fold compared to the control mice. Moreover, Matk/CHK deficiency led to significantly higher Pre-B cell colony formation following IL-7 stimulation. Interestingly, when mice received the in-vivo antigen challenge of TNP-Ovalbumin followed by re-stimulation, the Matk/CHK-/- lymph node and spleen cells produced significantly lower IFN- levels compared with the respective wild-type cells. Our study indicates that Matk/CHK is not functionally redundant with Csk, and that this tyrosine kinase plays an important role as a regulator of immunological responses. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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