scispace - formally typeset
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.

Papers
More filters
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.
Journal ArticleDOI

Massive Mitochondrial Degeneration in Motor Neurons Triggers the Onset of Amyotrophic Lateral Sclerosis in Mice Expressing a Mutant SOD1

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.
Journal ArticleDOI

Superoxide dismutase 1 with mutations linked to familial amyotrophic lateral sclerosis possesses significant activity

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.
Journal ArticleDOI

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.