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14 p, 2.3 MB SUMO-2 and PIAS1 modulate insoluble mutant huntingtin protein accumulation / O'Rourke, Jacqueline Gire (University of California) ; Gareau, Jaclyn R. (Sloan-Kettering Institute) ; Ochaba, Joseph (University of California) ; Song, Wan (University of California) ; Raskó, Tamás (Max-Delbrueck-Center for Molecular Medicine) ; Reverter i Cendrós, David (Sloan-Kettering Institute) ; Lee, John (University of Iowa) ; Mas Monteys, Alexandre (University of Iowa) ; Pallos, Judit (University of California) ; Mee, Lisa (University of California) ; Vashishtha, Malini (University of California) ; Apostol, Barbara L. (University of California) ; Nicholson, Thomas Peter (Enzo Life Sciences Ltd.) ; Illes, Katalin (University of California) ; Zhu, Ya-Zhen (University of California) ; Dasso, Mary (National Institute of Child Health and Development) ; Bates, Gillian P. (King's College London School of Medicine) ; Difiglia, Marian (Massachusetts General Hospital and Harvard Medical School) ; Davidson, Beverly (University of Iowa) ; Wanker, Erich E. (Max-Delbrueck-Center for Molecular Medicine) ; Marsh, J. Lawrence (University of California) ; Lima, Christopher D. (Sloan-Kettering Institute) ; Steffan, Joan S. (University of California) ; Thompson, Leslie M. (University of California.)
A key feature in Huntington disease (HD) is the accumulation of mutant Huntingtin (HTT) protein, which may be regulated by posttranslational modifications. Here, we define the primary sites of SUMOmodification in the amino-terminal domain of HTT, show modification downstream of this domain, and demonstrate that HTT is modified by the stress-inducible SUMO-2. [...]
2013 - 10.1016/j.celrep.2013.06.034
Cell Reports, Vol. 4, Issue 2 (July 2013) , p. 362-375  

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