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  • Title: Isolation of mutant T lymphocytes with defects in capacitative calcium entry.
    Author: Serafini AT, Lewis RS, Clipstone NA, Bram RJ, Fanger C, Fiering S, Herzenberg LA, Crabtree GR.
    Journal: Immunity; 1995 Aug; 3(2):239-50. PubMed ID: 7648396.
    Abstract:
    Calcium and calcium-binding proteins play important roles in the signaling cascade leading from the initial engagement of TCRs on T cells to the fully activated state. To undertake a molecular dissection of this cascade, we first isolated a Jurkat T cell line derivative containing the NF-AT promoter element driving transcription of the diphtheria toxin A chain gene (dipA), resulting in rapid cell death. Selecting viable cells that fail to activate NF-AT-dependent transcription, we isolated two independent cell lines possessing defects in capacitative Ca2+ entry. NF-AT-dependent transcription can be restored in these cells by expression of a constitutively active calcineurin, but not overexpression of the Ca2+ regulatory protein CAML, which can normally replace the Ca2+ signal. The defect in these cell lines probably lies between CAML and calcineurin in the T cell activation cascade.
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