Spinal Cord Injury Leads to Hyperoxidation and Nitrosylation of Skeletal Muscle Ryanodine Receptor-1 Associated with Upregulation of Nicotinamide Adenine Dinucleotide Phosphate Oxidase 4-Reference-Cited by-同舟云学术

Spinal Cord Injury Leads to Hyperoxidation and Nitrosylation of Skeletal Muscle Ryanodine Receptor-1 Associated with Upregulation of Nicotinamide Adenine Dinucleotide Phosphate Oxidase 4

Published:2017-06-15 Issue:12 Volume:34 Page:2069-2074
ISSN:0897-7151
Container-title:Journal of Neurotrauma
language:en
Short-container-title:Journal of Neurotrauma

Author:

Liu Xin-Hua¹²,Harlow Lauren¹,Graham Zachary A.¹²,Bauman William A.¹²³,Cardozo Christopher¹²³⁴

Affiliation:

1. National Center for the Medical Consequences of Spinal Cord Injury, James J. Peter VA Medical Center, Bronx, New York.

2. Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.

3. Department of Rehabilitation Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.

4. Department of Pharmacologic Science, Icahn School of Medicine at Mount Sinai, New York, New York.

Publisher

Mary Ann Liebert Inc

Subject

Clinical Neurology

Link

http://www.liebertpub.com/doi/pdf/10.1089/neu.2016.4763

Reference32 articles.

1. Early changes in muscle fiber size and gene expression in response to spinal cord transection and exercise

2. The molecular basis of skeletal muscle atrophy

3. Single muscle fiber size and contractility after spinal cord injury in rats

4. Ryanodine Receptors: Structure, Expression, Molecular Details, and Function in Calcium Release

5. Single channel measurements of the calcium release channel from skeletal muscle sarcoplasmic reticulum. Activation by Ca2+ and ATP and modulation by Mg2+.

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