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    Tec family kinases in T lymphocyte development and function

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    Authors
    Berg, Leslie J.
    Finkelstein, Lisa D.
    Lucas, Julie Ann
    Schwartzberg, Pamela L.
    UMass Chan Affiliations
    Department of Pathology
    Graduate School of Biomedical Sciences
    Document Type
    Journal Article
    Publication Date
    2005-03-18
    Keywords
    Animals; Antigens, CD28; Enzyme Activation; Humans; Mice; Models, Immunological; Molecular Structure; Protein Structure, Tertiary; Protein-Tyrosine Kinases; Receptors, Antigen, T-Cell; Signal Transduction; T-Lymphocytes
    Life Sciences
    Medicine and Health Sciences
    
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    Link to Full Text
    http://dx.doi.org/10.1146/annurev.immunol.22.012703.104743
    Abstract
    The Tec family tyrosine kinases are now recognized as important mediators of antigen receptor signaling in lymphocytes. Three members of this family, Itk, Rlk, and Tec, are expressed in T cells and activated in response to T cell receptor (TCR) engagement. Although initial studies demonstrated a role for these proteins in TCR-mediated activation of phospholipase C-gamma, recent data indicate that Tec family kinases also regulate actin cytoskeletal reorganization and cellular adhesion following TCR stimulation. In addition, Tec family kinases are activated downstream of G protein-coupled chemokine receptors, where they play parallel roles in the regulation of Rho GTPases, cell polarization, adhesion, and migration. In all these systems, however, Tec family kinases are not essential signaling components, but instead function to modulate or amplify signaling pathways. Although they quantitatively reduce proximal signaling, mutations that eliminate Tec family kinases in T cells nonetheless qualitatively alter T cell development and differentiation.
    Source
    Annu Rev Immunol. 2005;23:549-600. Link to article on publisher's site
    DOI
    10.1146/annurev.immunol.22.012703.104743
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/34309
    PubMed ID
    15771581
    Related Resources
    Link to article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.1146/annurev.immunol.22.012703.104743
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