Researchers at Fudan University in China and the Novartis Institutes for Biomedical Research in Boston, together with colleagues from the Baylor College of Medicine, Texas Children’s Hospital, Harvard Medical School, and Massachusetts General Hospital have reported using high-throughput screening to identify genes that modify endogenous mutant huntingtin protein (mHTT) and demonstrated that the overexpression of a particular gene product (negative regulator of ubiquitin-like protein 1 or NUB1, rescues mHTT-induced death in a fruit fly model system. The authors said that NUB1 reduces mHTT amounts by enhancing polyubiquination and proteasomal degradation of mHTT protein. The process requires CUL3 and the ubiquitin-like rotein NEDD8 necessary for CUL3 activation. The authors noted that interferon- lowered mHTT and rescued neuronal toxicity through induction of NUB1. The article on this research was published online on March 24, 2013 in Nature Neurology. [Nature Neurology abstract]
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