Key result
The frameshift mutation in atrial natriuretic peptide (fsANP) associated with familial atrial fibrillation markedly increases its half-life by rendering it resistant to proteolytic degradation.
Why the study?
Does the familial ANP mutation (fsANP) alter receptor interaction or proteolytic degradation compared to wild-type ANP?
Population
In vitro models including human natriuretic peptide receptors, kidney membranes, and purified neutral…
Comparison
Frameshift mutation product of atrial… vs Wild-type atrial natriuretic peptide (wtANP)
Design
Preclinical
Authors
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fsANP degradation resistance may drive familial AF; animal data leave open human therapeutic relevance.
Does the familial ANP mutation (fsANP) alter receptor interaction or proteolytic degradation compared to wild-type ANP?
The familial ANP mutation associated with atrial fibrillation leads to a peptide that is resistant to normal proteolytic degradation, explaining its elevated serum concentrations in affected patients.
Dickey et al. (2009) studied Familial atrial fibrillation. fsANP (frameshift mutant atrial natriuretic peptide) vs. wtANP (wild-type ANP) was evaluated on Receptor interaction and proteolytic degradation. The frameshift mutation in atrial natriuretic peptide (fsANP) associated with familial atrial fibrillation markedly increases its half-life by rendering it resistant to proteolytic degradation.
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