ARD1 stabilization of TSC2 suppresses tumorigenesis through the mTOR signaling pathway

• Published in: Science signaling Vol. 3; no. 108; p. ra9
• Main Authors: Kuo, Hsu-Ping, Lee, Dung-Fang, Chen, Chun-Te, Liu, Mo, Chou, Chao-Kai, Lee, Hong-Jen, Du, Yi, Xie, Xiaoming, Wei, Yongkun, Xia, Weiya, Weihua, Zhang, Yang, Jer-Yen, Yen, Chia-Jui, Huang, Tzu-Hsuan, Tan, Minjia, Xing, Gang, Zhao, Yingming, Lin, Chien-Hsing, Tsai, Shih-Feng, Fidler, Isaiah J, Hung, Mien-Chie
• Format: Journal Article
• Language: English
• Published: United States 09.02.2010
• Subjects: Acetyltransferases - metabolism; Alleles; Animals; Autophagy; Breast Neoplasms - genetics; Breast Neoplasms - metabolism; Cell Line, Tumor; Cell Proliferation; Gene Expression Profiling; Gene Expression Regulation, Neoplastic; Heterozygote; Humans; Mice; N-Terminal Acetyltransferase A; N-Terminal Acetyltransferase E; RNA, Small Interfering - metabolism; Signal Transduction; Tuberous Sclerosis Complex 2 Protein; Tumor Suppressor Proteins - metabolism

Mammalian target of rapamycin (mTOR) regulates various cellular functions, including tumorigenesis, and is inhibited by the tuberous sclerosis 1 (TSC1)-TSC2 complex. Here, we demonstrate that arrest-defective protein 1 (ARD1) physically interacts with, acetylates, and stabilizes TSC2, thereby repres...