Regulation of beta-actin gene transcription by insulin and phorbol esters.
Insulin and the phorbol ester, phorbol 12-myristate 13-acetate, induce beta-actin gene transcription in H4 cells. This occurred rapidly, with a maximum 15-fold stimulation following 15 min of insulin (5 x 10(-9) M) or phorbol ester (1 microgram/ml) exposure. The increase in beta-actin transcription was transitory, returning to baseline within 120 min. Pretreatment of cells with phorbol ester for 24 h, reducing functional protein kinase C activity, abolished the ability of phorbol esters to increase beta-actin transcription. When insulin was added to phorbol ester-pretreated cells the insulin-induced increase in beta-actin transcription was reduced by 40-60%. These findings support our hypothesis that a common regulatory signal is utilized by both insulin and phorbol esters for the complete induction of specific genes.
Messina
J L
JL
Department of Physiology, SUNY Health Science Center, Syracuse 13210.
Weinstock
R S
RS
D000199:Actins / Q000235:genetics*; D000818:Animals; D004305:Dose-Response Relationship, Drug; D005786:Gene Expression Regulation / Q000187:drug effects*; D066298:In Vitro Techniques; D007328:Insulin / Q000494:pharmacology*; D008113:Liver Neoplasms; D008114:Liver Neoplasms, Experimental; D011493:Protein Kinase C / Q000502:physiology; D051381:Rats; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology*; D013997:Time Factors; D014158:Transcription, Genetic / Q000187:drug effects; D014404:Tubulin / Q000235:genetics; D014407:Tumor Cells, Cultured
D000199:Actins; D007328:Insulin; D014404:Tubulin; D011493:Protein Kinase C; D013755:Tetradecanoylphorbol Acetate