Rapamycin inhibition of interleukin-2-dependent p33cdk2 and p34cdc2 kinase activation in T lymphocytes.

摘要: The immunosuppressant rapamycin (RAP) is a potent inhibitor of the entry interleukin (IL)-2-stimulated T cells into S-phase. Earlier results indicated that RAP treatment arrested growth murine IL-2-dependent cell line CTLL-2 in late G1-phase. To explore further interactions with cycle control machinery cells, we examined effects on activation cyclin-dependent kinases p34cdc2 and p33cdk2 G1-phase cells. Stimulation factor-deprived IL-2 led to assembly high molecular weight complexes containing active p33cdk2. appearance these was explained, at least part, by association both IL-2-induced cyclin A. profoundly inhibited A expression A-cyclin-dependent kinase IL-2-stimulated, Although largely dependent A, significant proportion pool complexed E. In contrast accumulation E only partially suppressed RAP, E-p33cdk2 were readily detected drug-treated These E-cyclin-dependent nonetheless devoid histone H1 activity. inhibitory E- A-associated suggest one or events participate regulation