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Mitochondrial Aconitase is a Transglutaminase 2 Substrate: Transglutamination is a Probable Mechanism Contributing to High-Molecular-Weight Aggregates of Aconitase and Loss of Aconitase Activity in Huntington Disease Brain

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Year: 2005
Type: article
Source: Neurochemical Research
DOI: 10.1007/s11064-005-8796-x
Authors: Soo-Youl Kim, Lyuben Marekov, Parvesh Bubber, Susan E. Browne, Irina Stavrovskaya, Jongmin Lee, Peter M. Steinert, John P. Blass, M. Flint Beal, Gary E. Gibson, Arthur J. L. Cooper
Institutions: Cornell University, Weill Cornell Medicine, National Institutes of Health, National Institute of Arthritis and Musculoskeletal and Skin Diseases, Burke Medical Research Institute, National Cancer Center
Language: English

Topic: Genetic Neurodegenerative Diseases
Subfield: Cellular and Molecular Neuroscience
Field: Neuroscience
Domain: Life Sciences
SDG: Good health and well-being

Open Access status: closed

Funders: National Institutes of Health, National Institute on Aging, National Institute of Mental Health
Awards: G1623524899, Mitochondiral enzymes/oxidative stress in Alzheimer's, Mitochondrial and Metabolic Dysfunction in Age-related Neurodegeneration, A National Resource for Postmortem Brain Research, G548514458
OpenAlex ID: W2017323564
FWCI: 0.603
Cites: 46
Cited by: 46
Related to: 10
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