ArticleBiochemistry2009
Impact of actin glutathionylation on the actomyosin-S1 ATPase.
Article in Biochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- Implications of S-glutathionylation of sarcomere proteins in cardiac disorders, therapies, and diagnosis.Frontiers in cardiovascular medicine · 2022Pooled it
- Redox and actin, a fascinating story.Redox biology · 2025Review
- From amino-acid to disease: the effects of oxidation on actin-myosin interactions in muscle.Journal of muscle research and cell motility · 2023Review
- Redox regulation of the actin cytoskeleton and its role in the vascular system.Free radical biology & medicine · 2017Review
- Actin filaments-A target for redox regulation.Cytoskeleton (Hoboken, N.J.) · 2016Review
- A change of heart: oxidative stress in governing muscle function?Biophysical reviews · 2015Article
- Emerging importance of oxidative stress in regulating striated muscle elasticity.Journal of muscle research and cell motility · 2015Review
- Redox-sensitive residue in the actin-binding interface of myosin.Biochemical and biophysical research communications · 2014Article
- Protein redox chemistry: post-translational cysteine modifications that regulate signal transduction and drug pharmacology.Frontiers in pharmacology · 2014Article
- Protein glutathionylation in cardiovascular diseases.International journal of molecular sciences · 2013Review
- Human heart failure is accompanied by altered protein kinase A subunit expression and post-translational state.Archives of biochemistry and biophysics · 2013Article
- Causes and consequences of cysteine S-glutathionylation.The Journal of biological chemistry · 2013Review
- Tropomyosin Ser-283 pseudo-phosphorylation slows myofibril relaxation.Archives of biochemistry and biophysics · 2013Article
- Oxidative stress and sarcomeric proteins.Circulation research · 2013Review
- Novel control of cardiac myofilament response to calcium by S-glutathionylation at specific sites of myosin binding protein C.Frontiers in physiology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Glutathionylation of intracellular proteins is an established physiological regulator of protein function. In multiple models, including ischemia-reperfusion of the heart, increased oxidative stress results in the glutathionylation of sarcomeric actin. We hypothesized that actin glutathionylation may play a role in the multifactorial change in cardiac muscle contractility observed during this pathophysiological state. Therefore, the functional impact of glutathionylated actin on the interaction with myosin-S1 was examined. Substituting glutathionylated F-actin for unmodified F-actin reduced the maximum actomyosin-S1 ATPase, and this was accompanied by an increase in the activation energy of the steady state ATPase. Measurement of steady state binding did not suggest a large impact of actin glutathionylation on the binding to myosin-S1. However, transient binding and dissociation kinetics determined by stopped-flow methods demonstrated that although actin glutathionylation did not significantly alter the rate constant of myosin-S1 binding, there was a significant decrease in the rate of ATP-induced myosin-S1 detachment in the presence of ADP. These results suggest that actin glutathionylation may play a limited but defined role in the alteration of contractility following oxidative stress to the myocardium, particularly through a decrease in the actomyosin ATPase activity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.