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Filipp, D., Moemeni, B., Ferzoco, A., Kathirkamathamby, K., Zhang, J., Ballek, O., Davidson, D., Veillette, A. and Julius, M. (2008) Lck-Dependent Fyn Activation Requires C-Terminus-Dependent Targeting of Kinase-Active Lck to Lipid Rafts. Journal of Biological Chemistry, 283, 26409-26422.
http://dx.doi.org/10.1074/jbc.M710372200

has been cited by the following article:

• TITLE: Fyn Expression Predicates Both Protective Immunity and Onset of Autoimmunity

  AUTHORS: Behrouz Moemeni, Nathalie Vacaresse, Marina Vainder, Michael E. Wortzman, Tania H. Watts, André Veillette, Thomas F. Gajewski, Michael Julius

  KEYWORDS: Fyn, Lck, TcR Signaling, Immunity, Autoimmunity

  JOURNAL NAME: Open Journal of Immunology, Vol.5 No.5, December 3, 2015

  ABSTRACT: Genomic disruption of Fyn has not been associated with an immune-deficient phenotype, notwithstanding the profound impairment in IL-2 production by T cells derived from Fyn-deficient animals observed in vitro. The results presented demonstrate that Fyn deficient animals succumb to influenza infection ahead of the protective expansion of lung infiltrating T cells and viral clearance observed in wild-type hosts. Formal proof that Fyn-dependent IL-2 production mediates T cell expansion in vivo is provided using a model of T cell induced enteropathy. Specifically, Fyn deficient naive T cells do not induce colitis in SCID animals due to their lack of expansion, and Fyn re-expression rescues both IL-2 production and its capacity to support in vivo expansion leading to colitis. These results reconcile the obligatory role of Fyn in T cell activation and autocrine IL-2 supported growth; and underscore the mechanism through which its function is integrated with and regulated by Lck.