Key result
The R213G mutation in extracellular-superoxide dismutase reduces its susceptibility to trypsin-like proteinases, with an IC50 of 0.15 microgram/ml (fivefold higher than normal EC-SOD).
Population
Healthy individuals and hemodialysis patients with and without the R213G mutation in human…
Comparison
Treatment with trypsin and neutrophil-release… vs Normal EC-SOD (n-EC-SOD)
Design
Preclinical
Authors
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May explain EC-SOD heparin affinity variation; leaves open relevance to human cardiovascular phenotypes.
Absolute Event Rate: 0.15% vs 0.03%
The R213G mutation in human EC-SOD confers resistance to trypsin-like proteinases, explaining the differences in heparin affinity of serum EC-SOD between individuals with and without the mutation.
Adachi et al. (1996) studied Healthy individuals and hemodialysis patients. R213G mutation in extracellular-superoxide dismutase (EC-SOD) vs. Normal EC-SOD (without R213G mutation) was evaluated on Susceptibility to trypsin (IC50 for heparin affinity). The R213G mutation in extracellular-superoxide dismutase reduces its susceptibility to trypsin-like proteinases, with an IC50 of 0.15 microgram/ml (fivefold higher than normal EC-SOD).
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