Inoki Ken, Guan Kun-Liang
Department of Molecular and Integrative Physiology, Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA.
Hum Mol Genet. 2009 Apr 15;18(R1):R94-100. doi: 10.1093/hmg/ddp032.
Tuberous sclerosis complex (TSC) is a relatively rare autosomal dominant disorder characterized by widespread benign tumor formation in a variety of organs. Mutations in either TSC1 or TSC2 tumor suppressor gene are responsible for TSC. The gene products of TSC1 and TSC2, also known as hamartin and tuberin, respectively, form a physical and functional complex and inhibit the mammalian target of rapamycin complex 1 (mTORC1) signaling. The mTORC1 pathway is an evolutionarily conserved growth promoting pathway. mTORC1 plays an essential role in a wide array of cellular processes including translation, transcription, trafficking and autophagy. In this review, we will discuss recent progresses in the TSC-mTOR field and their physiological functions and alterations of this pathway in pathophysiology.
结节性硬化症(TSC)是一种相对罕见的常染色体显性疾病,其特征是在多种器官中广泛形成良性肿瘤。TSC1或TSC2肿瘤抑制基因的突变是导致TSC的原因。TSC1和TSC2的基因产物分别称为错构瘤蛋白和结节蛋白,它们形成一个物理和功能复合体,并抑制雷帕霉素复合物1(mTORC1)信号通路。mTORC1途径是一种进化上保守的促进生长的途径。mTORC1在包括翻译、转录、运输和自噬在内的一系列细胞过程中起重要作用。在这篇综述中,我们将讨论TSC-mTOR领域的最新进展及其生理功能以及该途径在病理生理学中的改变。