中文摘要：

Glyceraldehyde-3-phosphate (GAPDH ) 被报导了与包含 polyglutamine (polyQ ) 的蛋白质交往领域。现在的学习被承担与 100Q 和 46Q 评估 polyQ 和 polyproline (息肉)领域的潜在的贡献到变异的狩猎的锡( htt )和N终端 htt ( 1-969 氨基酸)的 GAPDH.Overexpression 的合作本地化( htt1-969-100Q 和 httl-969-46Q ，变异的 htt )在人的乳腺癌 MCF-7 ，房间比 httl-969-18Q (野类型的 htt )的形成了更多的 htt 总数。有总数在在 N 终端 htt 表示息肉区域的变异然而并非野类型的 htt.Deletion 的房间被发现的 htt 的 GAPDH 的合作本地化没在 GAPDH 和变异的 htt 总数的合作本地化上有效果。这些结果建议 polyQ 领域，然而并非息肉领域，由 htt.This 效果可能贡献的异种在 GAPDH 的隐遁起一个作用到总数神经原的机能障碍在亨廷顿的疾病由变异的 htt 引起了。

英文摘要：

Glyceraldehyde-3-phosphate dehydrogenase （GAPDH） has been reported to interact with proteins containing the polyglutamine （polyQ） domain. The present study was undertaken to evaluate the potential contributions of the polyQ and polyproline （polyP） domains to the co-localization of mutant huntingtin （htt） and GAPDH. Overexpression of N-terminal htt （1-969 amino acids） with 100Q and 46Q （httl-969- 100Q and httl-969-46Q, mutant htt） in human mammary gland carcinoma MCF-7 cells formed more htt aggregates than that of httl-969-18Q （wild-type htt）. The co-localization of GAPDH with htt aggregates was found in the cells expressing mutant but not wild-type htt. Deletion of the polyP region in the N-terminal htt had no effect on the co-localization of GAPDH and mutant htt aggregates. These results suggest that the polyQ domain, but not the polyP domain, plays a role in the sequestration of GAPDH to aggregates by mutant htt. This effect might contribute to the dysfunction of neurons caused by mutant htt in Huntington＇s disease.