Cell Growth & Differentiation, Vol 1, Issue 8 345-350, Copyright © 1990 by American Association of Cancer Research

ARTICLES

Murine c-rel transcription is rapidly induced in T-cells and fibroblasts by mitogenic agents and the phorbol ester 12-O-tetradecanoylphorbol-13-acetate

RJ Grumont and S Gerondakis
Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Parkville, Victoria, Australia.

The c-rel protooncogene is here shown to be a member of the early response gene family. Expression induced by different agents is regulated by both transcriptional and posttranscriptional mechanisms. In quiescent fibroblasts, c-rel expression is maximally induced by serum or 12-O-tetradecanoylphorbol-13-acetate within 60 min and is superinduced in serum-stimulated fibroblasts by cycloheximide. In T-cells, although 12-O-tetradecanoylphorbol-13-acetate and concanavalin A both rapidly activate c-rel expression, the kinetics of induction mediated by these agents differs markedly. Nuclear run-on analysis demonstrates that induced c-rel expression is due primarily to increased transcription, and the rapid decrease in expression observed in serum- and 12-O-tetradecanoylphorbol-13-acetate-stimulated cells results from mRNA turnover. In the B-lymphoid lineage, c-rel is constitutively transcribed, with the differentiation stage-specific decrease in c-rel expression seen in plasmacytomas reflecting posttranscriptional regulation.

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