RETRACTED: The chromatin-remodeling complex WINAC targets a nuclear receptor to promoters and is impaired in Williams syndrome (Retracted article. See vol. 149, pg. 245, 2012)

被引:191
作者
Kitagawa, H
Fujiki, R
Yoshimura, K
Mezaki, Y
Uematsu, Y
Matsui, D
Ogawa, S
Unno, K
Okubo, M
Tokita, A
Nakagawa, T
Ito, T
Ishimi, Y
Nagasawa, H
Matsumoto, T
Yanagisawa, J
Kato, S
机构
[1] Univ Tokyo, Inst Mol & Cellular Biosci, Bunkyo Ku, Tokyo 1130032, Japan
[2] Univ Tokushima, Sch Med, Dept Internal Med 1, Tokushima 7708503, Japan
[3] Juntendo Univ, Sch Med, Dept Pediat, Bunkyo Ku, Tokyo 1138431, Japan
[4] Nagasaki Univ, Sch Med, Dept Biochem, Nagasaki 8528523, Japan
[5] Mitsubishi Kasei Inst Life Sci, Machida, Tokyo 1948511, Japan
[6] Univ Tokyo, Grad Sch Agr & Life Sci, Bunkyo Ku, Dept Appl Biol Chem, Tokyo 1130032, Japan
[7] SORST, Japan Sci & Technol, Kawaguchi, Saitama 3320012, Japan
关键词
D O I
10.1016/S0092-8674(03)00436-7
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
We identified a human multiprotein complex (WINAC) that directly interacts with the vitamin D receptor (VDR) through the Williams syndrome transcription factor (WSTF), WINAC has ATP-dependent chromatin-remodeling activity and contains both SWI/SNF components and DNA replication-related factors. The latter might explain a WINAC requirement for normal S phase progression. WINAC mediates the recruitment of unliganded VDR to VDR target sites in promoters, while subsequent binding of coregulators requires ligand binding. This recruitment order exemplifies that an interaction of a sequence-specific regulator with a chromatin-remodeling complex can organize nucleosomal arrays at specific local sites in order to make promoters accessible for coregulators. Furthermore, overexpression of WSTF could restore the impaired recruitment of VDR to vitamin D regulated promoters in fibroblasts from Williams syndrome patients. This suggests that WINAC dysfunction contributes to Williams syndrome, which could therefore be considered, at least in part, a chromatin-remodeling factor disease.
引用
收藏
页码:905 / 917
页数:13
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