TY - JOUR
T1 - T cell activation and increases in protein kinase C activity enhance retinoic acid-induced gene transcription
AU - Yang, Yili
AU - Minucci, Saverio
AU - Zand, Dina J.
AU - Ozato, Keiko
AU - Ashwell, Jonathan D.
PY - 1994/10
Y1 - 1994/10
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0028051982&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0028051982&partnerID=8YFLogxK
U2 - 10.1210/me.8.10.1370
DO - 10.1210/me.8.10.1370
M3 - Article
C2 - 7854354
AN - SCOPUS:0028051982
VL - 8
SP - 1370
EP - 1376
JO - Molecular Endocrinology
JF - Molecular Endocrinology
SN - 0888-8809
IS - 10
ER -