. Nuclear localization of N-terminal mutant huntingtin is cell cycle dependent. Eur J Neurosci. 2002 Jul;16(2):355-9. PubMed.

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  1. This is a lovely piece of work reporting that the specific nuclear localization of mutant htt (normal htt is mostly cytoplasmic) in neurons is cell cycle-dependent. The finding that N-terminal htt enters the nucleus only after cell cycle arrest may also explain the selective vulnerability of neurons in Huntington's disease. Because nuclear entry and aggregation of htt is critical to the pathogenesis of Huntington's disease, the mechanism of this cell cycle driven nuclear translocation needs to be explored. Cell cycle dysregulation has been proposed as a mechanism for neurodegeneration in Alzheimer's disease and certain other degenerative diseases. Perhaps the gain of function resulting from mutant htt may involve a similar dysregulation of the cell cycle in susceptible postmitotic neurons, leading to their death. The HD94 conditional mouse and neurons derived from it would be ideal models for pursuing such studies.

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