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Molecular Endocrinology, Vol 8, 1370-1376, Copyright © 1994 by Endocrine Society

ARTICLES

T cell activation and increases in protein kinase C activity enhance retinoic acid-induced gene transcription

Y Yang, S Minucci, DJ Zand, K Ozato and JD Ashwell
Laboratory of Immune Cell Biology, National Cancer Institute, Bethesda, Maryland 20892.

Retinoic acid (RA) has profound effects on cell growth and differentiation. Its receptors are members of the steroid/thyroid hormone receptor superfamily, which regulates nuclear transcription and gene expression by binding specific response elements. Protein kinase C (PKC) is activated during signal transduction initiated by a variety of membrane receptors. Using a RA-responsive element and reporter gene construct transfected into a T cell, we found: 1) T cell activation and PKC activators enhance transactivation by RA, 2) down-regulation of PKC protein has little effect on RA transactivation but abolishes superinduction by phorbol ester, which is restored by cotransfection of a PKC alpha-expression vector, and 3) cotransfection of dominant- negative c-jun does not prevent superinduction by phorbol ester. Together, these data demonstrate that PKC can modulate RA signal transduction, apparently without involvement of AP-1, and provide a new example of cross-talk between signal transduction pathways.


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