The inositol 1,4,5-trisphosphate receptor is essential for T-cell receptor signaling.

摘要: Abstract Antigen-specific activation of T lymphocytes, via stimulation the T-cell antigen receptor (TCR) complex, is marked by a rapid and sustained increase in concentration cytoplasmic free Ca2+ ([Ca2+]i). It has been suggested that second messenger inositol 1,4,5-trisphosphate (IP3) produced after TCR binds to IP3 (IP3R), an intracellular Ca(2+)-release channel, triggers [Ca2+]i activates transcription gene for growth factor interleukin 2 (IL-2). However, role IP3R signaling possibly plasma membrane influx cells remains unproven. Stable transfection (Jurkat) with antisense type 1 cDNA prevented expression, providing tool dissecting during activation. lacking failed or produce IL-2 stimulation. Moreover, depletion stores without stimulated IP3R. These results establish required release antigen-specific proliferation but not influx.