Dimer destabilization in superoxide dismutase may result in disease-causing properties: structures of motor neuron disease mutants. (Q37646220)

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26 December 2019

title

Dimer destabilization in superoxide dismutase may result in disease-causing properties: structures of motor neuron disease mutants (English)

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26 December 2019

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1

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26 December 2019

Svetlana Antonyuk

3

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26 December 2019

author name string

J Günter Grossmann

2

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26 December 2019

Richard W Strange

4

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26 December 2019

Peter A Doucette

5

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26 December 2019

Jorge A Rodriguez

6

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26 December 2019

Lisa J Whitson

7

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26 December 2019

P John Hart

8

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26 December 2019

Lawrence J Hayward

9

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26 December 2019

Joan Selverstone Valentine

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26 December 2019

S Samar Hasnain

11

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26 December 2019

language of work or name

English

0 references

publication date

31 March 2004

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Proceedings of the National Academy of Sciences of the United States of America

26 December 2019

published in

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26 December 2019

volume

101

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26 December 2019

issue

16

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26 December 2019

page(s)

5976-5981

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Refinement of macromolecular structures by the maximum-likelihood method

26 December 2019

cites work

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The structure of holo and metal-deficient wild-type human Cu, Zn superoxide dismutase and its relevance to familial amyotrophic lateral sclerosis

23 August 2017

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23 August 2017

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An alternative mechanism of bicarbonate-mediated peroxidation by copper-zinc superoxide dismutase: rates enhanced via proposed enzyme-associated peroxycarbonate intermediate

23 August 2017

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Familial amyotrophic lateral sclerosis mutants of copper/zinc superoxide dismutase are susceptible to disulfide reduction

23 August 2017

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Insights into Lou Gehrig's disease from the structure and instability of the A4V mutant of human Cu,Zn superoxide dismutase

23 August 2017

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Do oxidatively modified proteins cause ALS?

23 August 2017

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Role of superoxide dismutases in oxidative damage and neurodegenerative disorders

23 August 2017

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23 August 2017

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From Charcot to Lou Gehrig: deciphering selective motor neuron death in ALS

23 August 2017

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Current status of SOD1 mutations in familial amyotrophic lateral sclerosis

23 August 2017

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23 August 2017

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Use of TLS parameters to model anisotropic displacements in macromolecular refinement

23 August 2017

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Restoring low resolution structure of biological macromolecules from solution scattering using simulated annealing

23 August 2017

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Epidemiology of mutations in superoxide dismutase in amyotrophic lateral sclerosis

23 August 2017

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Motor neurons in Cu/Zn superoxide dismutase-deficient mice develop normally but exhibit enhanced cell death after axonal injury

23 August 2017

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Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosis

23 August 2017

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Amyotrophic lateral sclerosis and structural defects in Cu,Zn superoxide dismutase

23 August 2017

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Motor neuron degeneration in mice that express a human Cu,Zn superoxide dismutase mutation

23 August 2017

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

23 August 2017

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A frequent ala 4 to val superoxide dismutase-1 mutation is associated with a rapidly progressive familial amyotrophic lateral sclerosis

23 August 2017

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23 August 2017

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23 August 2017

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23 August 2017

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23 August 2017

Superoxide dismutases

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23 August 2017

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28 September 2017

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A familial amyotrophic lateral sclerosis-associated A4V Cu, Zn-superoxide dismutase mutant has a lower Km for hydrogen peroxide. Correlation between clinical severity and the Km value.

25 June 2018

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Familial amyotrophic lateral sclerosis-associated mutations decrease the thermal stability of distinctly metallated species of human copper/zinc superoxide dismutase

25 June 2018

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1 September 2018

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Human Cu/Zn superoxide dismutase (SOD1) overexpression in mice causes mitochondrial vacuolization, axonal degeneration, and premature motoneuron death and accelerates motoneuron disease in mice expressing a familial amyotrophic lateral sclerosis mut

1 September 2018

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An adverse property of a familial ALS-linked SOD1 mutation causes motor neuron disease characterized by vacuolar degeneration of mitochondria

1 September 2018

1 reference

PubMed

https://pubmed.ncbi.nlm.nih.gov/15056757

inferred from PubMed ID database lookup

12 December 2020

based on heuristic

Accumulation of neurofilaments and SOD1-immunoreactive products in a patient with familial amyotrophic lateral sclerosis with I113T SOD1 mutation

1 reference

PubMed

https://pubmed.ncbi.nlm.nih.gov/15056757

inferred from PubMed ID database lookup

12 December 2020

based on heuristic

Identifiers

DOI

10.1073/PNAS.0305143101

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26 December 2019

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26 December 2019

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