Pyridoxamine protects protein backbone from oxidative fragmentation
نویسندگان
چکیده
منابع مشابه
Pyridoxamine protects proteins from functional damage by 3-deoxyglucosone: mechanism of action of pyridoxamine.
Pyridoxamine (PM) is a promising drug candidate for treatment of diabetic nephropathy. The therapeutic effect of PM has been demonstrated in multiple animal models of diabetes and in phase II clinical trials. However, the mechanism of PM therapeutic action is poorly understood. One potential mechanism is scavenging of pathogenic reactive carbonyl species (RCS) found to be elevated in diabetes. ...
متن کاملPyridoxamine scavenges protein carbonyls and inhibits protein aggregation in oxidative stress-induced human HepG2 hepatocytes.
Introduction of carbonyl groups into amino acid residues is a hallmark for oxidative damage to proteins by reactive oxygen species (ROS). Protein carbonylation can have deleterious effects on cell function and viability, since it is generally unrepairable by cells and can lead to protein dysfunction and to the production of potentially harmful protein aggregates. Meanwhile, pyridoxamine (PM) is...
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Protein misfolding and aggregation have been associated with the onset of neurodegenerative disorders. Recent studies demonstrate that the aggregation process can result in a high diversity of protein conformational states, however the identity of the specific species responsible for the cellular damage is still unclear. Here, we use yeast as a model to systematically analyse the intracellular ...
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Accurate flow of genetic information from DNA to protein requires faithful translation. An increased level of translational errors (mistranslation) has therefore been widely considered harmful to cells. Here we demonstrate that surprisingly, moderate levels of mistranslation indeed increase tolerance to oxidative stress in Escherichia coli. Our RNA sequencing analyses revealed that two antioxid...
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ژورنال
عنوان ژورنال: Biochemical and Biophysical Research Communications
سال: 2011
ISSN: 0006-291X
DOI: 10.1016/j.bbrc.2011.06.188