Population
Recombinant human cardiac L-type Ca2+ channel alpha1C subunits stably expressed in human embryonic kidney…
Comparison
Redox agents and hypoxia vs Untreated cells or cells treated with…
Design
Preclinical
Authors
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Redox modulation of distinct cysteines may mediate hypoxic Ca channel inhibition in cardiac models; leaves open human relevance and therapeutic translation.
Distinct cysteine residues on the human cardiac L-type Ca2+ channel alpha1C subunit undergo redox modulation, which alters channel function and mediates hypoxic inhibition.
Fearon et al. (1999) studied this question.
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