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.