结节性硬化症:遗传与物理分析之间。

D J Halley
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引用次数: 11

摘要

结节性硬化症(TSC)是一种常染色体显性多系统疾病,具有广泛的临床变异性。目前对TSC流行率的估计表明,它可能超过1:6 000。新的突变是经常发生的,因为大约三分之二的病例显然是散发的。基因座异质性已建立,一个基因位于染色体9q34 (TSC1)上,另一个基因位于染色体16p13.3 (TSC2)上。大多数TSC2突变可能是细微的改变。在某些情况下,体细胞和种系嵌合体可能是家族内表型变异和明显的非外显性的解释。预测的蛋白产物tuberin在生长抑制中的作用将与在TSC患者肿瘤中观察到的等位基因丢失一致。利用针对该蛋白不同部分的抗体对tuberin进行研究,有望深入了解其正常和受损的功能。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Tuberous sclerosis: between genetic and physical analysis.

Tuberous sclerosis complex (TSC) is an autosomal dominant multisystem disorder with extensive clinical variability. Present estimates of the prevalence of TSC suggest that it may exceed 1:6,000. New mutations are frequent, as about 2/3 of all cases are apparently sporadic. Locus heterogeneity has been established, with one gene on chromosome 9q34 (TSC1) and the other on chromosome 16p13.3 (TSC2). The majority of TSC2 mutations are probably subtle alterations. In some cases, somatic and germline mosaicism might be explanations for intrafamilial phenotype variation and apparent non penetrance. A role of the predicted protein product tuberin in growth suppression would be in agreement with allelic losses observed in tumors of TSC patients. Studies on tuberin using antibodies raised against various parts of the protein can be expected to provide insight into its normal and impaired function.

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