Isolation of mutant T lymphocytes with defects in capacitative calcium entry

Andrew T. Serafini, Richard S. Lewis, Neil A. Clipstone, Richard J. Bram, Christopher Fanger, Steve Flering, Leonard A. Herzenberg, Gerald R. Crabtree

Research output: Contribution to journalArticlepeer-review

57 Scopus citations


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 by 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.

Original languageEnglish (US)
Pages (from-to)239-250
Number of pages12
Issue number2
StatePublished - Aug 1995

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases


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