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S-Glutathiolation by peroxynitrite activates SERCA during arterial relaxation by nitric oxide
Nitric oxide (NO) physiologically stimulates the sarco/endoplasmic reticulum calcium (Ca2+) ATPase (SERCA) to decrease intracellular Ca2+ concentration and relax cardiac, skeletal and vascular smoothExpand
SOD1 mutations disrupt redox-sensitive Rac regulation of NADPH oxidase in a familial ALS model.
TLDR
It is demonstrated that SOD1 is not just a catabolic enzyme, but can also directly regulate NADPH oxidase-dependent (Nox-dependent) O(2)(*-) production by binding Rac1 and inhibiting its GTPase activity. Expand
Protein modification during biological aging: selective tyrosine nitration of the SERCA2a isoform of the sarcoplasmic reticulum Ca2+-ATPase in skeletal muscle.
TLDR
The age-dependent functional and chemical modifications of the rat skeletal-muscle sarcoplasmic-reticulum (SR) Ca2+-ATPase isoforms SERCA1 and SERCA2a from fast-twitch and slow-twitch muscle respectively are characterized in detail. Expand
Peroxynitrite modification of protein thiols: oxidation, nitrosylation, and S-glutathiolation of functionally important cysteine residue(s) in the sarcoplasmic reticulum Ca-ATPase.
TLDR
It is determined by HPLC-MS that the modification of one (out of 24) Cys residue of the sarcoplasmic reticulum (SR) Ca-ATPase isoform SERCA1, Cys(349), by peroxynitrite is sufficient for the modulation of enzyme activity. Expand
Methionine oxidation by reactive oxygen species: reaction mechanisms and relevance to Alzheimer's disease.
  • C. Schöneich
  • Chemistry, Medicine
  • Biochimica et biophysica acta
  • 17 January 2005
TLDR
Detailed mechanistic schemes for the reactions of various prominent, biologically relevant ROS with methionine and organic model sulfides are provided, characterizing the physico-chemical parameters, which control this mechanism, and its physiological relevance, specifically for the oxidation and neurotoxicity of the Alzheimer's disease beta-amyloid peptide (betaAP). Expand
3-Nitrotyrosine modification of SERCA2a in the aging heart: a distinct signature of the cellular redox environment.
TLDR
It is shown that the additional loss of activity in the senescent Fischer 344 rat heart relative to that of young adult hearts is a result of increased 3-nitrotyrosine modification of the Ca-ATPase, and age-dependent increases in nitration of cardiac SERCA2a are identified using multiple analytical methods. Expand
Chemical instability of protein pharmaceuticals: Mechanisms of oxidation and strategies for stabilization.
TLDR
Careful screening of chelating agents has been shown to be an alternative method for preventing metal-catalyzed oxidation, a site-specific process, in which the addition of antioxidants may accelerate the oxidation reaction. Expand
Proteomic identification of 3-nitrotyrosine-containing rat cardiac proteins: effects of biological aging.
TLDR
Cardiac proteins from whole heart homogenate and heart mitochondria of Fisher 344/Brown Norway F1 rats are identified, consistent with age-dependent increased oxidative stress and with free radical-dependent damage of proteins. Expand
Oxidative degradation of pharmaceuticals: theory, mechanisms and inhibition.
TLDR
The present article reviews mechanistic details of autoxidation and chain oxidation processes, as well as the oxidation of selected functional groups commonly affected in drugs. Expand
Diastereoselective reduction of protein‐bound methionine sulfoxide by methionine sulfoxide reductase
TLDR
It is reported for the first time that pMSR selectively reduces the D‐sulfoxide diastereomer of CaM‐bound L‐MetSO (L‐Met‐D‐SO) and the accumulation of MetSO upon oxidative stress and aging in vivo may be related to incomplete, diastsereoselective, repair by pMSr. Expand
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