Article
A functional deficiency of TERA/VCP/p97 contributes to impaired DNA repair in multiple polyglutamine diseases.
Nature communications - 1 Jan 2013
Fujita Kyota, Nakamura Yoko, Oka Tsutomu, Ito Hikaru, Tamura Takuya, Tagawa Kazuhiko, Sasabe Toshikazu, Katsuta Asuka, Motoki Kazumi, Shiwaku Hiroki, Sone Masaki, Yoshida Chisato, Katsuno Masahisa, Eishi Yoshinobu, Murata Miho, Taylor J Paul, Wanker Erich E, Kono Kazuteru, Tashiro Satoshi, Sobue Gen, La Spada Albert R, Okazawa Hitoshi
Abstract excerpt
It is hypothesized that a common underlying mechanism links multiple neurodegenerative disorders. Here we show that transitional endoplasmic reticulum ATPase (TERA)/valosin-containing protein (VCP)/p97 directly binds to multiple polyglutamine disease proteins (huntingtin, ataxin-1, ataxin-7 and androgen receptor) via polyglutamine sequence. Although normal and mutant polyglutamine proteins interact with...
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