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- W1982362034 abstract "To investigate the effect of Bcl-2 on Ca2+ signaling in T cells, we continuously monitored Ca2+ concentration in Bcl-2–positive and –negative clones of the WEHI7.2 T cell line after T cell receptor (TCR) activation by anti-CD3 antibody. In Bcl-2–negative cells, high concentrations of anti-CD3 antibody induced a transient Ca2+ elevation, triggering apoptosis. In contrast, low concentrations of anti-CD3 antibody induced Ca2+ oscillations, activating the nuclear factor of activated T cells (NFAT), a prosurvival transcription factor. Bcl-2 blocked the transient Ca2+ elevation induced by high anti-CD3, thereby inhibiting apoptosis, but did not inhibit Ca2+ oscillations and NFAT activation induced by low anti-CD3. Reduction in the level of all three inositol 1,4,5-trisphosphate (InsP3) receptor subtypes by small interfering RNA inhibited the Ca2+ elevation induced by high but not low anti-CD3, suggesting that Ca2+ responses to high and low anti-CD3 may have different requirements for the InsP3 receptor. Therefore, Bcl-2 selectively inhibits proapoptotic Ca2+ elevation induced by strong TCR activation without hindering prosurvival Ca2+ signals induced by weak TCR activation." @default.
- W1982362034 created "2016-06-24" @default.
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- W1982362034 date "2006-01-02" @default.
- W1982362034 modified "2023-10-16" @default.
- W1982362034 title "Bcl-2 differentially regulates Ca2+ signals according to the strength of T cell receptor activation" @default.
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- W1982362034 doi "https://doi.org/10.1083/jcb.200506189" @default.
- W1982362034 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2063540" @default.
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