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Abstract
The phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) and the calcium ionophore ionomycin differentially regulated the expression of the gamma-T-cell antigen receptor (gamma-TCR) gene in human thymocytes. Ionomycin induced an increase in gamma-TCR mRNA while TPA prevented this effect. The effects of ionomycin and TPA are completely reversed upon their removal. Protein kinase C-depleted cells are unable to respond to TPA but the induction of gamma-TCR by ionomycin was unimpaired. The regulation of gamma-TCR gene expression by TPA and ionomycin occurred at the level of gene transcription, whereas the rate of gamma-TCR mRNA degradation was unaffected by TPA or ionomycin.
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