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

Yili Yang, Saverio Minucci, Dina J. Zand, Keiko Ozato, Jonathan D. Ashwell

Research output: Contribution to journalArticlepeer-review

Abstract

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 PKCα-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.

Original languageEnglish
Pages (from-to)1370-1376
Number of pages7
JournalMolecular Endocrinology
Volume8
Issue number10
DOIs
Publication statusPublished - Oct 1994

ASJC Scopus subject areas

  • Molecular Biology
  • Endocrinology, Diabetes and Metabolism

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