Modulation of mutant Huntingtin aggregates and toxicity by human myeloid leukemia factors

详细信息    查看全文

• 作者：Manisha Banerjee ; ¹ ; ^{manisha.banerjee@gmail.com} ; ^{manishab@barc.gov.in} ; Moumita Datta² ; Nitai P. Bhattacharyya ; ³ ; ^{nitai.bhattacharyya@gmail.com}
• 关键词：HTT ; Huntingtin ; MLF ; myeloid leukemia factor ; HD ; Huntington&rsquo ; s disease ; Poly Q ; polyglutamine ; GFP ; green fluorescent protein ; FRAP ; fluorescence recovery after photo bleaching ; RFI ; relative fluorescence intensity ; CREB ; cAMP response element-binding protein
• 刊名：The International Journal of Biochemistry & Cell Biology
• 出版年：2017
• 出版时间：January 2017
• 年：2017
• 卷：82
• 期：Complete
• 页码：1-9
• 全文大小：2588 K
• 卷排序：82

文摘

Human myeloid leukemia factors were found to interact preferentially with mutant N-terminal Huntingtin protein. Human myeloid leukemia factors significantly reduced mutant HTT aggregates and subsequent apoptosis in Neuro2A cells. Human myeloid leukemia factors significantly altered the mobile state of mutant Huntingtin aggregates. In the presence of exogenous MLF1, transcription factors like p53, TBP, CREB were released from the mutant HTT aggregates. Over all data provides support for the “sequestered poly Q hypothesis” proposed earlier.