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Papers In Press, published online ahead of print November 22, 2000
Vollum Institute, Oregon Health Sciences Institute, Portland, OR 97201
Corresponding Author: goodmanr{at}ohsu.edu
CREM
J. Biol. Chem, 10.1074/jbc.M008274200
Submitted on September 10, 2000
Revised on November 21, 2000
Accepted on November 22, 2000
Cooperative mechanism of transcriptional activation by a CREM
mutant containing a motif for constitutive binding to CBP
is a transcription factor that is highly related to CREB, but represses cAMP-induced gene expression from simple artificial promoters containing a cAMP-response element (CRE). CREM lacks two glutamine-rich Q regions that, in CREB, are thought to be necessary for transcriptional activation. Nevertheless, protein kinase A (PKA) stimulation induces CREM to activate the complex native promoter in the phosphoenolpyruvate carboxykinase (PEPCK) gene. To study this phenomenon in the absence of PKA stimulation, we introduced a mutation into CREM to allow constitutive binding to the coactivator CREB-Binding Protein (CBP). This mutant, CREMDIEDML, constitutively activated the PEPCK promoter. By engineering the leucine zipper regions of CREMDIEDML and CREBDIEDML to direct their patterns of dimerization, we found that only CREMDIEDML homodimers fully activated the PEPCK promoter. By using a series of deletion and block mutants of the PEPCK promoter, we found that activation by CREMDIEDML depended on the CRE and two C/EBP sites. A dominant negative inhibitor of C/EBP, A-C/EBP, suppressed activation by CREMDIEDML. Furthermore, a GAL4-C/EBP fusion protein and CREMDIEDML cooperatively activated a promoter containing three GAL4 sites and the PEPCK CRE. Thus, we propose that the C/EBP sites in the PEPCK promoter allow CREM to activate transcription despite its lack of Q regions.
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