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      Discovery of a Novel, Potent, and Src Family-selective Tyrosine Kinase Inhibitor : STUDY OF Lck- AND FynT-DEPENDENT T CELL ACTIVATION

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          Most cited references 27

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          Single step method of RNA isolation by acid guanidium thiocyanate phenol chloroform extraction. Anal

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            Tyrosine kinase inhibition: an approach to drug development.

             A Levitzki,  A Gazit (1995)
            Protein tyrosine kinases (PTKs) regulate cell proliferation, cell differentiation, and signaling processes in the cells of the immune system. Uncontrolled signaling from receptor tyrosine kinases and intracellular tyrosine kinases can lead to inflammatory responses and to diseases such as cancer, atherosclerosis, and psoriasis. Thus, inhibitors that block the activity of tyrosine kinases and the signaling pathways they activate may provide a useful basis for drug development. This article summarizes recent progress in the development of PTK inhibitors and demonstrates their potential use in the treatment of disease.
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              Genetic evidence for the involvement of the lck tyrosine kinase in signal transduction through the T cell antigen receptor.

              Signaling through the T cell antigen receptor (TCR) results both in rapid increases in tyrosine phosphorylation on a number of proteins and in the activation of the phosphatidylinositol pathway. It is not clear how stimulation of the TCR leads to these signaling events. Mutants of the Jurkat T cell line have been previously isolated that fail to show increases in calcium following receptor stimulation. Analysis of one of these mutants, JCaM1, which is defective in the induction of tyrosine phosphorylation, revealed a defect in the expression of functional lck tyrosine kinase. The lack of lck activity was caused in part by a splicing defect. Expression of the lck cDNA in JCaM1 restores the ability of the cell to respond to TCR stimulation. These results indicate that lck is required for normal signal transduction through the TCR.
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                Author and article information

                Journal
                Journal of Biological Chemistry
                J. Biol. Chem.
                American Society for Biochemistry & Molecular Biology (ASBMB)
                0021-9258
                1083-351X
                January 12 1996
                January 12 1996
                : 271
                : 2
                : 695-701
                Article
                10.1074/jbc.271.2.695
                © 1996
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