肿瘤中hamartin和tuberin的不同分布以及核糖体S6激酶的磷酸化增加  

Differential localization of hamartin and tuberin and increased S6 phosphorylati on in a tuber

作　　者：Jansen F.E. Notenboom R.G.E. Nellist M. O. Van Nieuwenhuizen 高方 

机构地区：[1]Department of Child Neurology, University Medical Ce nter Utrecht, PO Box 85090, 3508 AB Utrecht, Netherlands Dr.

出　　处：《世界核心医学期刊文摘（神经病学分册）》2005年第3期57-57,共1页Digest of the World Core Medical Journals:Clinical Neurology

摘　　要：In a tuberous sclerosis patient with a mutation in the TSC1 tumor suppressor g ene, no second hit mutation was found in a resected cortical tuber. Tuber giant cells showed predominantly nuclear hamartin, cytosolic tuberin, and hyperphosph orylation of S6. Differential accumulation of hamartin and tuberin in separate c ellular compartments of giant cells may prevent formation of the hamartin tuber in complex, resulting in increased S6 phosphorylation. These data provide an alt ernative mechanism for tuberogenesis.In a tuberous sclerosis patient with a mutation in the TSC1 tumor suppressor g ene, no second hit mutation was found in a resected cortical tuber. Tuber giant cells showed predominantly nuclear hamartin, cytosolic tuberin, and hyperphosph orylation of S6. Differential accumulation of hamartin and tuberin in separate c ellular compartments of giant cells may prevent formation of the hamartin tuber in complex, resulting in increased S6 phosphorylation. These data provide an alt ernative mechanism for tuberogenesis.

关 键 词：S6 HAMARTIN TUBERIN 结节性脑硬化 抑癌基因 瘤巨细胞 细胞腔 

分 类 号：R730.2[医药卫生—肿瘤]