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1 ng that the RANTES-activated channel was the Ca2+ -activated K+ channel.
2 ng machinery in eukaryotic large-conductance Ca2+ activated K+ channels.
3 ing that it was carried by large-conductance Ca2+ activated K+ channels.
4 a selective inhibitor of large-conductance, Ca2+-activated K+ channels.
5 ediated through actions on large-conductance Ca2+-activated K+ channels.
6 on of apamin, a potent antagonist of SK-type Ca2+-activated K+ channels.
7 reviously discovered blocker of voltage- and Ca2+-activated K+ channels.
8 of charybdotoxin-sensitive large conductance Ca2+-activated K+ channels.
9 involve the activation of large conductance Ca2+-activated K+ channels.
10 g to inward-rectifier, voltage-activated, or Ca2+-activated K+ channels.
11 red low [Ca2+]i mainly through its effect on Ca2+-activated K+ channels.
12 y dependent on membrane hyperpolarization by Ca2+-activated K+ channel activation, with apparently le
13 inct from those of Kv1 and large-conductance Ca2+-activated K+ channels (also present at the FS cell
14 of human coronary arterioles via opening of Ca2+-activated K+ channels and hyperpolarization of VSMC
15 duced following blockade of apamin-sensitive Ca2+-activated K+ channels and provide further support f
16 es the open probability of large conductance Ca2+-activated K+ channels and results in smooth muscle
17 by tetraethylammonium (TEA),an inhibitor of Ca2+-activated K+ channels, and by high [K+]0 (20 mmol/L
18 activates the large conductance voltage and Ca2+-activated K+ channel (BK) expressed in a heterologo
20 gested that activation of large conductance, Ca2+-activated K+ channels (BKCa) provides an opposing h
22 r apamin (10(-7) mol/L), a small-conductance Ca2+-activated K+ channel blocker, inhibited both dilati
23 xin (CTX; 10(-8) mol/L), a large-conductance Ca2+-activated K+ channel blocker, or apamin (10(-7) mol
25 g the alpha-subunit of the large conductance Ca2+-activated K+ channel, cslo-alpha, was expressed in
26 hanges in the amplitude of large-conductance Ca2+-activated K+ channel current recorded on-cell from
27 llular K+ gradients caused by efflux through Ca2+-activated K+ channels expressed in Chinese hamster
29 ated KCNN4, represent the small conductance, Ca2+-activated K+ channel (Gardos channel) in human red
31 of sulfhydryl redox reagents on human brain Ca2+-activated K+ channels (hslo) expressed in both huma
32 f the Na+/Ca2+ exchanger (NCX), intermediate Ca2+-activated K+ channels (IK(Ca)), or cystic fibrosis
33 t cells express the intermediate conductance Ca2+-activated K+ channel iKCa1, which opens following I
34 10(-8) mol/L, a blocker of large-conductance Ca2+-activated K+ channels) impaired dilation to AA (19+
35 ET increased the open-state probability of a Ca2+-activated K+ channel in coronary smooth muscle cell
36 e (SKCa) and intermediate-conductance (IKCa) Ca2+-activated K+ channels in endothelial cells leads to
38 rtical neurons, inhibiting large-conductance Ca2+-activated K+ channels in TC neurons can lead to fas
41 or null mutation of 1 of a small conductance Ca2+-activated K+ channel isoform, SK2 channel, and demo
42 that the interplay between Ca2+ currents and Ca2+-activated K+ channels (KCa channels) is important f
45 y found that MTMR6 specifically inhibits the Ca2+-activated K+ channel, KCa3.1, by dephosphorylating
47 ced cDNAs derived from cslo, which encodes a Ca2+-activated K+ channel like those shown to help deter
50 st that apamin-sensitive, small-conductance, Ca2+-activated K+ channels may play an important role in
51 fects of DCEBIO, an intermediate conductance Ca2+-activated K+ channel modulator, and the effects of
52 These results suggest that RANTES opens the Ca2+ -activated K+ channels of EoL-1 cells through activ
53 T) blocks directly and with high potency the Ca2+-activated K+ channels of human erythrocytes, erythr
56 channels provide direct evidence that these Ca2+-activated K+ channels play important roles in IC ne
61 a specific blocker of the small-conductance Ca2+-activated K+ channel (sK(Ca)) When cells were pre-t
65 onfirmed the presence of a small conductance Ca2+-activated K+ channel subtype (SK2) in human and mou
69 BAPTA series Ca2+ buffers can activate those Ca2+-activated K+ channels that underlie the slow AHP, w
70 ived from the plasma membrane Ca2+-pump, the Ca2+-activated K+-channel, the Ca2+/CaM-dependent kinase
71 smooth muscle by activating big conductance Ca2+-activated K+ channels to produce spontaneous transi
73 K1 and SK3 subtypes of the small conductance Ca2+-activated K+ channels were significantly decreased,
74 ce P (0.03-0.1 microM), or block of SK or BK Ca2+-activated K+ channels with apamin (100 nM) or charb
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