Expansion of the polyQ repeats in THAP11 forms intranuclear aggregation and causes cell G0/G1 arrest.
作者： Rong-Hua Yin , Yang Li , Fan Yang , Yi-Qun Zhan , Miao Yu
DOI: 10.1002/CBIN.10255
关键词:
摘要: Polyglutamine diseases are a group of neurodegenerative disorders caused by expansion CAG repeat that encodes polyglutamine in each respective disease gene. The transcription factor THAP11, member THAP family, is involved cell growth, ES pluripotency and embryogenesis. Previous studies suggest THAP11 protein contains 29-residue motif the number ranges from 20 to 41 Indian population. We have investigated numbers at locus normal individuals patients Chinese Han population 38Q (THAP11(38Q)) was found patients. Using fluorescence confocal-based imaging, THAP11(38Q) formed intranuclear inclusions easier than THAP11(29Q) PC12 cells. Enhanced toxicity THAP11(38Q)-expressing cells growth inhibition G0/G1 arrest. CREB-mediated activity inhibited THAP11(38Q). factor, TBP, coactivator CBP, chaperon protein, HSP70, could be recruited These results indicate forms intracellular aggregation toxic cells, suggesting putative role disease.
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