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TSC1和TSC2:在人类遗传性疾病结节性硬化症中发生突变的基因。

TSC1 and TSC2: genes that are mutated in the human genetic disorder tuberous sclerosis.

作者信息

Sampson J R

机构信息

Institute of Medical Genetics, University of Wales College of Medicine, Heath Park, Cardiff CF14 8XN, UK.

出版信息

Biochem Soc Trans. 2003 Jun;31(Pt 3):592-6. doi: 10.1042/bst0310592.

Abstract

The tuberous sclerosis complex genes TSC1 and TSC2 were first identified by positional cloning strategies in the heritable human disorder tuberous sclerosis. They encode previously unknown proteins, termed hamartin and tuberin respectively, that form a functional complex. The phenotypic manifestations of tuberous sclerosis are extremely diverse and suggest normal roles for TSC1 and TSC2 in regulating the growth, proliferation, migration and differentiation of many cell types. Investigations of TSC1 and TSC2 in a number of model organisms and cell-culture systems have provided new insights into the mechanisms through which these roles are effected. Most promisingly, the hamartin-tuberin complex has been shown to function as a negtive regulator of the insulin receptor/phosphoinositide 3-kinase/S6 kinase pathway. Drugs that act to inhibit this pathway may have therapeutic potential for tuberous sclerosis and the related disorder lymphangioleiomyomatosis.

摘要

结节性硬化症相关基因TSC1和TSC2最初是通过定位克隆策略在遗传性人类疾病结节性硬化症中被鉴定出来的。它们分别编码此前未知的蛋白质,即错构瘤蛋白和结节蛋白,这两种蛋白形成一个功能复合体。结节性硬化症的表型表现极为多样,这表明TSC1和TSC2在调节多种细胞类型的生长、增殖、迁移和分化方面具有正常作用。在多种模式生物和细胞培养系统中对TSC1和TSC2的研究,为这些作用得以实现的机制提供了新的见解。最有前景的是,错构瘤蛋白-结节蛋白复合体已被证明作为胰岛素受体/磷酸肌醇3激酶/S6激酶通路的负调节因子发挥作用。作用于抑制该通路的药物可能对结节性硬化症及相关疾病淋巴管平滑肌瘤病具有治疗潜力。

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