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S phase progression. WINAC mediates the recruitment Hirochika Kitagawa,1,2 Ryoji Fujiki,1 Kimihiro Yoshimura,1 Yoshihiro Mezaki,1 Yoshikatsu Uematsu,1 Daisuke Matsui,1 Satoko Ogawa,1 Kiyoe Unno,1,3 Mataichi Okubo,3 Akifumi Tokita,3 Takeya Nakagawa,4 Takashi Ito,4 Yukio Ishimi,5 of unliganded VDR to VDR target sites in promoters, Hiromichi Nagasawa,6 Toshio Matsumoto,2 while subsequent binding of coregulators requires liJunn Yanagisawa,1,7 and Shigeaki Kato1,7,* gand binding. This recruitment order exemplifies that Institute of Molecular and Cellular Biosciences an interaction of a sequence-specific regulator with a University of Tokyo chromatin-remodeling complex can organize nucleo1-1-1 Yayoi somal arrays at specific local sites in order to make Bunkyo-ku promoters accessible for coregulators. Furthermore, Tokyo 113-0032 overexpression of WSTF could restore the impaired Japan recruitment of VDR to vitamin D regulated promoters 2 First Department of Internal Medicine in fibroblasts from Williams syndrome patients. This University of Tokushima School of Medicine suggests that WINAC dysfunction contributes to 3-18-15 Kuramoto-cho Williams syndrome, which could therefore be considTokushima 770-8503 ered, at least in part, a chromatin-remodeling factor Japan disease. 3 Department of Pediatrics

Retraction Notice to: The Chromatin-Remodeling Complex WINAC Targets a Nuclear Receptor to Promoters and Is Impaired in Williams Syndrome