Although expansion of a polyglutamine tract in the huntingtin protein is known to cause Huntington's disease (HD), there is considerable debate as to how this mutation leads to the selective neuronal loss that characterizes the disease. The observation that mutant huntingtin accumulates in neuronal nuclei has led to the hypothesis that the molecular mechanism may involve the disruption of specific nuclear activities. Recently, several nuclear interaction partners for huntingtin have been identified, including HypA, a splicing factor-like protein of unknown function.
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