Oxidatively modified proteins in aging and disease.
By M. Beal. Free Radical Biology & Medicine, 2002
803 citations recorded by the source corpus.
Subfields: Molecular Biology, Neurology, Physiology
View Paper: https://www.semanticscholar.org/paper/eab82d883c0c3d36d33c192e64e76cb2e6382d49
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Citations in the corpus
- Oxidative stress in ALS: key role in motor neuron injury and therapeutic target. (2010, background): “the mitochondrial respiratory chain, and is believed to be a major cause of aging [45–47].”
- Stress response, cell death and signalling: the many faces of reactive oxygen species (2003, background): “The hazards of reactive oxygen species (ROS) have long been recognized, as has their role in disease and ageing in animals (Beal 2002, Melov 2002, Perry et al. 2002).”
- Mechanism of Oxidative Stress in Neurodegeneration (2012, background): “Protein oxidative damage in the form of protein carbonyls [13] is also evident in PD brain compared to controls, and there is some evidence to suggest a role for nitration and nitrosylation of certain proteins due to reactive nitrogen species in PD brain [14].”
- Physiological implications of hydrogen sulfide: a whiff exploration that blossomed. (2012, background): “Excessive ONOO production (as 3-nitrotyrosine) is a trademark of various neurodegenerative diseases (38).”
- Glutathione dysregulation and the etiology and progression of human diseases (2009, background): “Environmental toxicants have long been hypothesized to play a dominant role in the sporadic cases of Parkinson's disease, and oxidative stress has been proposed as a major mechanism of cell death in Parkinson's disease (Beal, 2002; Jenner, 2003).”
- Mitochondrial creatine kinase in human health and disease. (2006, positive): “Most of the reactive species originate directly or indirectly from the activity of the mitochondrial respiratory chain, in particular under conditions of increased oxidative stress like ischemia/reperfusion injury, neurodegenerative disease, or aging [108,120,121].”
- Oxidative Stress and the Pathogenesis of Alzheimer's Disease (2013, background): “The excessive reactive oxygen species may be generated from mechanisms such as mitochondria dysfunction and/or aberrant accumulation of transition metals, while the abnormal accumulation of Abeta and tau proteins appears to promote the redox imbalance.”
- Protein carbonyl groups as biomarkers of oxidative stress. (2003, background): “Similarly, the presence of 3nitrotyrosine in proteins is thought to be a relatively specific marker of oxidative damage mediated by peroxynitrite [9].”