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. 1993 Feb;4(2):173-84.
doi: 10.1091/mbc.4.2.173.

Increased intracellular Ca2+ induces Ca2+ influx in human T lymphocytes

D M Haverstick  1 , L S Gray
Affiliations
Free PMC article

Increased intracellular Ca2+ induces Ca2+ influx in human T lymphocytes

D M Haverstick et al. Mol Biol Cell. 1993 Feb.
Free PMC article

Abstract

One current hypothesis for the initiation of Ca2+ entry into nonelectrically excitable cells proposes that Ca2+ entry is linked to the state of filling of intracellular Ca2+ stores. In the human T lymphocyte cell line Jurkat, stimulation of the antigen receptor leads to release of Ca2+ from internal stores and influx of extracellular Ca2+. Similarly, treatment of Jurkat cells with the tumor promoter thapsigargin induced release of Ca2+ from internal stores and also resulted in influx of extracellular Ca2+. Initiation of Ca2+ entry by thapsigargin was blocked by chelation of Ca2+ released from the internal storage pool. The Ca2+ entry pathway also could be initiated by an increase in the intracellular concentration of Ca2+ after photolysis of the Ca(2+)-cage, nitr-5. Thus, three separate treatments that caused an increase in the intracellular concentration of Ca2+ initiated Ca2+ influx in Jurkat cells. In all cases, Ca(2+)-initiated Ca2+ influx was blocked by treatment with any of three phenothiazines or W-7, suggesting that it is mediated by calmodulin. These data suggest that release of Ca2+ from internal stores is not linked capacitatively to Ca2+ entry but that initiation is linked instead by Ca2+ itself, perhaps via calmodulin.

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References

    1. J Gen Physiol. 1967 Jan;50(3):583-601 - PubMed
    1. Cell. 1992 May 29;69(5):715-8 - PubMed
    1. Prostaglandins. 1984 Apr;27(4):553-62 - PubMed
    1. Proc Natl Acad Sci U S A. 1984 Jul;81(13):4169-73 - PubMed
    1. Proc Natl Acad Sci U S A. 1984 Aug;81(15):4955-9 - PubMed

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