Characterization of PHA and anti-T3 induced transduction mechanisms in a human T-cell leukaemia line.
Stimulation of the T-cell line JURKAT with PHA or anti-T3 antibody leads to a rapid and sustained rise of cytosolic free Ca2+, as determined by quin2 fluorescence measurements. Pertussis toxin and N-ethylmaleimide, substances known to inactivate a regulatory N-protein, caused partial to complete inhibition of the cytosolic free Ca2+ response induced both by anti-T3 or PHA. The high cytosolic free Ca2+ level induced by anti-T3 or PHA declined more rapidly after addition of phorbol ester, phorbol myristate acetate (PMA). PMA did not affect cytosolic free Ca2+ changes induced by ionomycin indicating that the effect of PMA is due to a direct inhibitory effect on a transduction mechanism and not to activation of Ca2+ extrusion. Our data suggest that a regulatory N-protein is involved in the transduction of the PHA and anti-T3 response into a rapid and sustained elevation of cytosolic free Ca2+. Activation of protein kinase C by PMA modulates the calcium response in JURKAT cells, suggesting that protein kinase C may be involved in feedback regulation of the transduction mechanism.
D002118:Calcium / Q000378:metabolism; D002460:Cell Line; D003600:Cytosol / Q000378:metabolism; D005033:Ethylmaleimide / Q000494:pharmacology; D006801:Humans; D007938:Leukemia / Q000235:genetics / Q000276:immunology*; D037342:Pertussis Toxin; D010835:Phytohemagglutinins / Q000494:pharmacology*; D013601:T-Lymphocytes / Q000276:immunology*; D014161:Transduction, Genetic; D010566:Virulence Factors, Bordetella / Q000494:pharmacology
D010835:Phytohemagglutinins; D010566:Virulence Factors, Bordetella; D037342:Pertussis Toxin; D005033:Ethylmaleimide; D002118:Calcium