Functional categorization of the 55 induced genes revealed that most were either related to carbon metabolism, membrane proteins, or were involved in oxidoreduction reactions.
1
Their versatility, which arises from an ability to undergo reduction-oxidation chemistry, enables them to act as critical cofactors of enzymes throughout the cell.
2
Reactive oxygen species, generated by reduction-oxidation (redox) reactions, have been recognized as one of the major mediators of ischemia and reperfusion injury in the brain.
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Reduction-oxidation (redox) signaling systems are emerging as important targets in pancreatic cancer.
1
Iron-sulfur clusters are prosthetic groups commonly found in proteins that participate in oxidation-reduction reactions and catalysis.
2
The N-terminus of MTRR containing a conserved domain of FMNRed is closely concerned with the oxidation-reduction process.
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The mutated proteins show spectral properties similar to those of the wild-type enzyme, in all oxidation-reduction states.
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This is in accord with the high oxidation-reduction potential of the flavin, which thermodynamically stabilizes the reduced enzyme.
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In comparison, 27 proteins were up-regulated in dark-cutting beef related to oxidation-reduction processes, muscle contraction, and oxidative phosphorylation.
1
This cyclic redoxreaction of the metal generates OH.
2
Taken together these data demonstrate that H296 is responsible for proton exchange in the redoxreaction.
3
Flavin-based electron-bifurcation is a mechanism that couples an exergonic redoxreaction to an endergonic one allowing energy conservation in anaerobic microorganisms.
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This provides mass spectrometric evidence for the mechanism of the nitro to amine conversion process during nitroreduction, an important redoxreaction involved in carcinogenesis.
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Re-evaluating these previous data we here discuss a mechanism, by which the redoxreaction of N2 induces conformational changes possibly leading to proton translocation.
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However, the identity of most redox-regulated mitochondrial proteins remains to be defined.
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This process obviates the need for exogenous enzymes and redox mediator supplements.
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These findings reveal a new layer of nitroso-redox imbalance in dystrophic cardiomyopathy.
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These single-domain flavoenzymes display redox potentials compatible with electron transfer between partners.
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Hence, there is interest in redox and metabolic modulators as anticancer agents.
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In addition, the redox properties of the Te functionalities have been explored.
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Blood free radical concentration was reduced, that is, CV improved redox homeostasis.
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Manipulation of redox signaling may be beneficial in cancer patients receiving trastuzumab.
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Solution and solid state CV studies revealed the redox-active characteristics of the complexes.
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The redox balance in the renal cell seems, therefore, of the utmost importance.
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CSK therefore provides a redox regulatory mechanism that couples photosynthesis to gene expression.
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These markers play important roles in redox regulations throughout the body.
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Importantly, disruption of redox organization is a common basis for disease.
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The redox-sensitive transcription factors AP-1 and NF-kappaB have been implicated in these effects.
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These results define a novel redox-based mechanism to propagate Fas-dependent apoptosis.
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This redox cycle may constitute the principal physiologic function of bilirubin.