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Submitted on March 15, 2004
Accepted on September 22, 2004
Laboratory of Endocrine Cell Biology, Department of Internal Medicine, Chungnam National University College of Medicine, Deajeon 301-721 Korea. Keimyung University School of Medicine, 194 Dongsan-Dong, Jung-Gu, Daegu 700-712, Korea. Hormone Research Center, School of Biological Sciences and Technology, Chonnam National University, Kwangju, 500-757, Korea. Department of Oncology, Lombardi Cancer Center, Georgetown University Medical Center, 3970 Reservoir Road, NW, Washington, DC 20057, USA
* To whom correspondence should be addressed. E-mail: hsc{at}chonnam.ac.kr.
CR6 interacting factor 1 (CRIF1) was recently identified as a nuclear protein that interacts with the Gadd45 (growth arrest and DNA damage inducible 45) family of proteins and participates in the regulation of the G1/S phase of the cell cycle. However, the nuclear action of CRIF1 is largely unknown. In this study, we demonstrate that CRIF1 acts as a novel co-regulator of transactivation of the orphan nuclear receptor Nur77. Both in vitro and in vivo studies show that CRIF1 interacts with Nur77 via the Nur77 AB domain and that it dramatically inhibits the AB domain-mediated transactivation of Nur77. Transient transfection assays demonstrate that CRIF1 inhibits SRC-2-mediated Nur77 transactivation, and silencing of endogenous CRIF1 by siRNA relieves this repression. CRIF1 posseses intrinsic repressor activities that are not affected by the histone deacetylase inhibitor Trichostatin A. In addition, over-expression of CRIF1 inhibits thyroid stimulating hormone/protein kinase A-induced NurRE promoter activitity. CRIF1 inhibited Nur77-dependent induction of E2F1 promoter activity, mRNA expression, and Nur77-mediated G1/S progression in cell cycle. These results suggest that CRIF1 acts as a repressor of the orphan nuclear receptor Nur77 by inhibiting AB domain-mediated transcriptional activitity.
NURSA Molecule Pages Link:
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