Mechanisms and residues responsible for slow activation and Ba 2+ block of the cardiac
muscarinic K+ channel, Kir3. 1/Kir3. 4, were investigated using site-directed mutagenesis.
Mutagenesis of negatively charged residues located throughout the pore of the channel (in
H5, M2, and proximal C terminus) reduced or abolished slow activation. The strongest
effects resulted from mutagenesis of residues in H5 close to the selectivity filter; mutagenesis
of residues in M2 and proximal C terminus equivalent to those identified as important …