Z
Zuoshang Xu
Researcher at University of Massachusetts Medical School
Publications - 91
Citations - 13662
Zuoshang Xu is an academic researcher from University of Massachusetts Medical School. The author has contributed to research in topics: SOD1 & Amyotrophic lateral sclerosis. The author has an hindex of 51, co-authored 84 publications receiving 12942 citations. Previous affiliations of Zuoshang Xu include Johns Hopkins University School of Medicine & Johns Hopkins University.
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Journal ArticleDOI
Asymmetry in the assembly of the RNAi enzyme complex.
TL;DR: It is shown that the two strands of an siRNA duplex are not equally eligible for assembly into RISC, and it is suggested that single-stranded miRNAs are initially generated as siRNA-like duplexes whose structures predestine one strand to enter the RISC and the other strand to be destroyed.
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Massive Mitochondrial Degeneration in Motor Neurons Triggers the Onset of Amyotrophic Lateral Sclerosis in Mice Expressing a Mutant SOD1
Jiming Kong,Zuoshang Xu +1 more
TL;DR: The absence of massive motor neuron death at the early stages of the disease indicates that the majority of motor neurons could be rescued after clinical diagnosis, and indicates that mutant SOD1 toxicity is mediated by damage to mitochondria in motor neurons.
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Superoxide dismutase 1 with mutations linked to familial amyotrophic lateral sclerosis possesses significant activity
David R. Borchelt,Michael K. Lee,Hilda S. Slunt,Michael Guarnieri,Zuoshang Xu,Philip C. Wong,Robert H. Brown,Donald L. Price,Sangram S. Sisodia,Don W. Cleveland +9 more
TL;DR: For mutants such as G37R, either surprisingly modest losses in activity (involving only the mutant subunit) can yield motor neuron death, or alternatively, mutant SOD1 may acquire properties that injure motor neurons by one or more mechanisms unrelated to the metabolism of oxygen radicals.
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Increased expression of neurofilament subunit NF-L produces morphological alterations that resemble the pathology of human motor neuron disease
TL;DR: Transgenic mice that accumulate NF-L to approximately 4-fold the normal level in the sciatic nerve indicate that extensive accumulation of neurofilaments in motor neurons can trigger the neurodegenerative process.
Journal ArticleDOI
Mutations in the Profilin 1 Gene Cause Familial Amyotrophic Lateral Sclerosis
Chi Hong Wu,Claudia Fallini,Nicola Ticozzi,Pamela Keagle,Peter C. Sapp,Peter C. Sapp,Katarzyna Piotrowska,Patrick Lowe,Max Koppers,Diane McKenna-Yasek,Desiree M. Baron,Jason E. Kost,Paloma Gonzalez-Perez,Andrew Fox,Jenni Adams,Franco Taroni,Cinzia Tiloca,Ashley Lyn Leclerc,Shawn C. Chafe,Dev Mangroo,Melissa J. Moore,Jill A. Zitzewitz,Zuoshang Xu,Leonard H. van den Berg,Jonathan D. Glass,Gabriele Siciliano,Elizabeth T. Cirulli,David Goldstein,François Salachas,Vincent Meininger,Wilfried Rossoll,Antonia Ratti,Cinzia Gellera,Daryl A. Bosco,Gary J. Bassell,Vincenzo Silani,Vivian E. Drory,Robert H. Brown,John Landers +38 more
TL;DR: It is shown that mutations within the profilin 1 (PFN1) gene can cause FALS, and cytoskeletal pathway alterations contribute to ALS pathogenesis.