Wild-type and mutant SOD1 share an aberrant conformation and a common pathogenic pathway in ALS

被引：0

作者：

Daryl A Bosco

Gerardo Morfini

N Murat Karabacak

Yuyu Song

Francois Gros-Louis

Piera Pasinelli

Holly Goolsby

Benjamin A Fontaine

Nathan Lemay

Diane McKenna-Yasek

Matthew P Frosch

Jeffrey N Agar

Jean-Pierre Julien

Scott T Brady

Robert H Brown

机构：

[1] University of Massachusetts Medical Center,Department of Neurology

[2] University of Illinois at Chicago,Department of Anatomy and Cell Biology

[3] Brandeis University,Department of Chemistry

[4] Laval University,Department of Psychiatry and Neuroscience

[5] Research Centre of CHUQ,undefined

[6] Weinberg Unit for ALS Research,undefined

[7] Farber Institute for the Neurosciences,undefined

[8] Thomas Jefferson University,undefined

[9] C.S. Kubik Laboratory for Neuropathology,undefined

[10] Massachusetts General Hospital,undefined

[11] Marine Biological Laboratory,undefined

来源：

Nature Neuroscience | 2010年 / 13卷

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学科分类号：

摘要：

Could similar changes in SOD1 underlie both familial and sporadic ALS? Here, Bosco et al. find that wild-type SOD1 from sporadic ALS tissues shows conformational changes similar to those seen in familial ALS and that aberrant wild-type SOD1 can be pathogenic, potentially as a result of the same SOD1-dependent mechanism seen in familial ALS.

引用

页码：1396 / 1403

页数：7

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