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    Proc Natl Acad Sci U S A. 1987 Oct;84(19):6879-83.

    Isolation and characterization of a T-lymphocyte somatic mutant with altered signal transduction by the antigen receptor.

    Source

    Howard Hughes Medical Institute, Department of Medicine, University of California, San Francisco 94143.

    Abstract

    We have developed an approach for deriving and characterizing antigen-receptor (CD3/Ti) signal-transduction mutants. This strategy combines receptor-mediated growth inhibition and fluorescence-activated cell sorting with the Ca2+-indicator indo-1. Despite the expression of structurally normal CD3/Ti complexes, one such mutant (J.CaM1) fails to exhibit inositolphospholipid metabolism or Ca2+ mobilization in response to anti-CD3 or anti-Ti monoclonal antibodies and fails to produce lymphokines in response to these antibodies. Surprisingly, anti-Ti antibody retains its effectiveness as a stimulus for the down-regulation of CD3/Ti surface expression. These cells remain responsive to AIF-4, at least one anti-CD3 antibody, and some combinations of nonagonist anti-Ti and anti-CD3 antibodies. The mutation in J.CaM1 appears to lie in a proximal component of the signal-transduction apparatus.

    PMID:
    3309950
    [PubMed - indexed for MEDLINE]
    PMCID:
    PMC299188
    Free PMC Article

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