Cellular Thiols Redox Status: a Switch for NF-κB Activation During Myocardial Post-ischaemic Reperfusion
- 31 August 2002
- journal article
- Published by Elsevier in Journal of Molecular and Cellular Cardiology
- Vol. 34 (8), 997-1005
- https://doi.org/10.1006/jmcc.2002.2046
Abstract
No abstract availableKeywords
This publication has 27 references indexed in Scilit:
- Intracellular oxidation/reduction status in the regulation of transcription factors NF-κB and AP-1Toxicology Letters, 1999
- Molecular Mechanisms of Neutrophil-Endothelial Cell Adhesion Induced by Redox ImbalanceCirculation Research, 1999
- Mechanisms by which IκB proteins control NF-κB activityProceedings of the National Academy of Sciences, 1999
- Inhibition of nuclear factor κB attenuates proinflammatory cytokine and inducible nitric-oxide synthase expression in postischemic myocardiumBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 1998
- Reactive Oxygen Species as Mediators of Signal Transduction in Cardiovascular DiseaseTrends in Cardiovascular Medicine, 1998
- Induction of nuclear factor κB and activation protein 1 in postischemic myocardiumFEBS Letters, 1997
- Metabolic Adaptation During a Sequence of No-Flow and Low-Flow IschemiaCirculation, 1996
- Rapid proteolysis of IκB-α is necessary for activation of transcription factor NF-κBNature, 1993
- Intracellular thiols regulate activation of nuclear factor kappa B and transcription of human immunodeficiency virus.Proceedings of the National Academy of Sciences, 1990
- Occurrence of oxidative stress during reperfusion of the human heart.Circulation, 1990