Key points are not available for this paper at this time.
Design
Review
Answers are grounded in this paper and cite their sources.
Structural features of maxi-K(Ca) channels support molecular models of excitability; leaves open therapeutic targeting in cardiovascular disease.
Large-conductance, voltage-, and Ca(2+)-sensitive K(+) (maxi-K(Ca)) channels regulate neuronal and smooth muscle excitability. Their pore-forming alpha-subunit shows similarities with voltage-gated channels and indeed can open in the practical absence of Ca(2+). The NH(2) terminus is unique, with a seventh transmembrane segment involved in beta-subunit modulation. The long COOH terminus is implied in Ca(2+) modulation.
No takes yet. Share an insight, caveat, or question.
Toro et al. (1998) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: