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1 to a well-characterized pore blocker of the BK channel.
2 ncreases calcium-dependent activation of the BK channel.
3 ion permeation gate at the cytosolic side of BK channel.
4 effect of beta4 on kinase modulation of the BK channel.
5 lectively disrupts ethanol modulation of the BK channel.
6 close apposition of ryanodine receptors and BK channels.
7 ls, which in turn are specifically linked to BK channels.
8 blished, little is known about how they open BK channels.
9 y of recombinant and prostate adenocarcinoma BK channels.
10 1 reduced the membrane surface expression of BK channels.
11 g was used to assess functionality of mutant BK channels.
12 acological inhibitors or shRNA knock-down of BK channels.
13 ividual VGCCs, of A-type VGKCs and of SK and BK channels.
14 al, depression of excitability via clustered BK channels.
15 g the pore of heterologously expressed human BK channels.
16 isengagement of the gamma1-F273S mutant from BK channels.
17 2+)- and voltage-gated (Slo1) big potassium (BK) channel.
18 a(2+)-activated, and voltage dependent K(+) (BK) channels.
19 the activity of Ca(2+)-activated potassium (BK) channels.
20 the activity of Ca(2+)-activated potassium (BK) channels.
21 ant two-pore domain (K2P) and big potassium (BK) channels.
22 alcium- and voltage-dependent big potassium (BK) channels.
23 uctance, voltage- and Ca(2+)-activated K(+) (BK) channels.
24 mal large-conductance Ca(2+)-activated K(+) (BK) channels, a critical negative feedback mechanism tha
25 cortical/medullary collecting duct, whereas BK channel abundance increased in principal cells of the
26 mSlo1 and further developed a model in which BK channels act as a calcium sensor capable of quantitat
27 n mallotoxin and the gamma subunits in their BK channel-activating effects in membrane patches excise
28 oteolysis, leading to the down-regulation of BK channel activation and impaired coronary function in
30 angement allows tight tracking between local BK channel activation and the gating of CaV1.3 channels
31 ugh direct interaction, how ethanol-mediated BK channel activation causes behavioral intoxication is
36 llosterically coupled to each other, control BK channel activity and are potential targets for regula
38 determine the significance of smooth muscle BK channel activity for blood pressure regulation, we in
39 unit surface trafficking controls functional BK channel activity in arterial myocytes and vascular co
42 nockout (dKO) mice to genetically upregulate BK channel activity in the absence of FMRP and determine
45 C mice, implying that impaired smooth muscle BK channel activity lowers blood pressure in these anima
47 ur studies thus suggest that upregulation of BK channel activity normalizes multi-level deficits caus
51 vel large-conductance Ca(2+)-activated K(+) (BK) channel agonist that shifts the activation V1/2 of t
52 ysosomal storage diseases (LSDs) and whether BK channel agonists rescue abnormal lysosomal storage in
53 s expressing both alpha- and beta1-subunits, BK channel alpha-subunits were endogenously S-acylated.
54 arge-conductance Ca(2+)-activated potassium (BK) channel alpha and auxiliary beta1 subunits that are
55 m channels), recent findings have shown that BK channels also contribute to inhibition in basal, high
56 of large conductance Ca(2+)-activated K(+) (BK) channels also result in tremor and motor disorders.
57 role of MuRF1 in the regulation of vascular BK channel and coronary function has not been examined.
58 tion, surface trafficking of beta1 subunits, BK channel and transient BK current activation, and vaso
59 ced reduction of whole cell BK currents, and BK channels and ANG-II receptors were found to co-locali
60 flash photolysis of caged Ca(2+) to activate BK channels and determine their intrinsic sensitivity to
61 s of CaV1.3 channels surrounding clusters of BK channels and forming a multi-channel complex both in
62 -frequency (apical) OHCs that do not express BK channels and from immature high-frequency OHCs before
63 echanism by which a vasoconstrictor inhibits BK channels and identify Rab11A serine 177 as a modulato
65 ntains functional coupling between RyR2s and BK channels and is critically important for cerebral art
66 In certain ligand-gated channels, such as BK channels and MthK, a Ca(2+)-activated K(+) channel fr
67 lization of calcium channels with respect to BK channels and presynaptic release components significa
71 rge-conductance calcium-activated potassium (BK) channels and Kv3.3 voltage-gated potassium channels
72 ), voltage- and calcium-activated potassium (BK) channels and their modulatory beta-subunits are able
73 he channel through the central cavity of the BK channel, and that only a single PAX molecule can inte
74 alling pathways such as K(+) release through BK channels, and the production and release of arachidon
75 rge-conductance calcium-activated potassium (BK) channels, and this effect is mediated through the cA
77 eases in mIPSC frequency by either selective BK channel antagonists or ethanol were not accompanied w
78 ltage clamp, and their response to selective BK channel antagonists, channel activators, or ethanol w
80 corded from high-frequency OHCs that express BK channels are briefer than IPSCs recorded from low-fre
82 e-conductance Ca(2+)- and voltage-gated Slo1 BK channels are directly activated by nanomolar levels o
85 der high-calorie conditions, suggesting that BK channels are promising drug targets for pharmacothera
88 arge-conductance calcium-activated potassium BK channels are widely expressed in the brain and are in
89 big conductance calcium-activated potassium (BK) channel are preferentially expressed by electrosenso
91 ctance calcium (Ca)(2+)-activated potassium (BK) channels are functionally significant modulators of
92 ductance Ca(2+)- and voltage-activated K(+) (BK) channels are involved in a large variety of physiolo
93 uctance voltage- and calcium-activated K(+) (BK) channels are key physiological players in muscle, ne
94 ce calcium- and voltage-activated potassium (BK) channels are potently modified by their functional c
95 arge conductance Ca(2+)-activated potassium (BK) channels are S-acylated at two sites that impart dis
97 dependent and calcium-activated K(+) (MaxiK, BK) channels are widely expressed in many tissues and or
98 ge-gated K(+) channels of large conductance (BK channels) are expressed in a diverse variety of both
100 The functional expression of both VGCCs and BK channels, as well as their localization with respect
103 ppeared to be mediated through activation of BK channels, because the effects of ML-SA1 on Tat-mediat
104 eted mouse model with global ablation of the BK channel (BK(L1/L1)) and adipocyte-specific BK-deficie
106 Furthermore, following bath application of BK channel blockers for 10 min, ethanol failed to furthe
108 spike frequency, a mechanism independent of BK channels but dependent on background non-selective co
109 In arterial smooth muscle, ANG-II inhibits BK channels, but the underlying molecular mechanisms are
110 iary gamma1-3 subunits potently modulate the BK channel by shifting its voltage-dependence of channel
112 ominent slow C-type inactivation/recovery in BK channels by an extreme low concentration of extracell
113 gest METH exposure decreased the activity of BK channels by decreasing BK-alpha subunit levels at the
114 veal an all-or-none functional regulation of BK channels by gamma-subunits: channels either exhibit a
116 rdation protein (FMRP) and that FMRP acts on BK channels by modulating the channel's gating kinetics.
118 We found that METH decreased the activity of BK channels by stimulating BK-alpha subunit trafficking.
122 rface beta1 subunits leads to a reduction in BK channel calcium-sensitivity, inhibition of transient
123 t cations sensed by a large structure in the BK channel called the "gating ring," which is formed by
124 the cells with blockers of either the NSC or BK channels, caused a strong inhibition of the A23187-in
126 uctance, calcium- and voltage-activated K(+)(BK) channel consists of the pore-forming alpha subunits
129 nductance Ca(2+) and voltage-activated K(+) (BK) channels control membrane excitability in many cell
130 /voltage-gated, large conductance potassium (BK) channels control numerous physiological processes, i
131 ethanol on GABA release and that presynaptic BK channels could serve as a target for ethanol effects
133 Ca(2+)-activated and voltage-dependent K(+) (BK) channels, critical for mucociliary function in the a
135 ibition of S-acylation attenuated endogenous BK channel currents independently of changes in cell sur
137 de that functional effects of S-acylation on BK channels depend on the presence of beta1-subunits.
138 an BK channel rescued intoxication and other BK channel-dependent behaviors in a slo-1-null mutant ba
139 T352I mutant BK channel selectively rescued BK channel-dependent behaviors while conveying resistanc
140 This mutation did not interfere with other BK channel-dependent behaviors, suggesting that the muta
141 We here identify, for the first time, a BK channel-dependent molecular synaptic mechanism leadin
142 hat of large conductance, Ca(2+)-gated K(+) (BK) channels despite the lack of sequence similarity.
143 e of the mechanisms responsible for creating BK channel diversity fundamental to the adequate functio
145 ch-clamp recordings confirmed that the human BK channel engineered with the T352I missense mutation w
146 On the other hand, activating TRPML1 and BK channels enhanced cellular degradation of exogenous T
147 The large conductance Ca(2+)-activated K(+) (BK) channel, expressed abundantly in vascular smooth mus
149 for BK channels, viral-mediated increases in BK channel expression in SCA1 Purkinje neurons improves
151 studies in Xenopus oocytes that co-expressed BK channel-forming (cbv1) and accessory beta1 subunits c
152 big conductance Ca(2+)-activated potassium (BK) channel forms a physical and functional coupling wit
154 e protein, promotes the trafficking of SLO-1 BK channels from the ER to the plasma membrane by shield
155 latory gamma subunits, LRRC26 and LRRC52, to BK channel function and localization in mouse IHCs.
156 ght the importance of not only CFTR but also BK channel function in maintaining ASL homeostasis and e
159 a on aldosterone regulation by renal/adrenal BK channel function, BKbeta1(-/-) strain A mice have inc
161 ownregulates CFTR activity but also inhibits BK channel function, thereby causing ASL depletion.
169 ne KCNMA1, encoding the alpha-subunit of the BK channel have emerged as responsible for a variety of
170 ce lacking the pore-forming alpha-subunit of BK channels have longer IPSCs than do the OHCs of BKalph
171 nductance voltage and Ca(2+)-activated K(+) (BK) channel have a key role in the ethanol effect on GPe
173 s expression system, Mel activates the human BK channel (hSlo1) in a membrane-delimited manner in the
175 ermined (i) a basic extracellular map of the BK channel, (ii) beta1-subunit-induced rearrangements of
179 how that 1) LINGO1 coimmunoprecipitated with BK channels in human brain, 2) coexpression of LINGO1 an
181 In summary, we demonstrate a novel role for BK channels in regulating glutamatergic transmission and
184 big conductance Ca(2+)-activated potassium (BK) channel in regulating endolysosome pH, as well as Ta
185 ce calcium- and voltage-activated potassium (BK) channels in spontaneous and secretagogue-induced act
186 conductance calcium- and voltage-activated (BK) channels in spontaneous and secretagogue-induced act
188 ce voltage- and calcium-activated potassium (BK) channels inhibiting channel activity independently o
189 requency-current (f-I) relationship, whereas BK channel inhibition had little effect on the f-I slope
190 n to iberiotoxin and vasodilation to NS1619, BK channel inhibitors and activators, respectively.
191 effect on GPe neurons, as the application of BK channel inhibitors blocked the ethanol-induced firing
193 emains unclear, however, to what extent FMRP-BK channel interactions contribute to synaptic and circu
194 to evoke the observed voltage waveform, the BK channel is functionally redundant whereas hERG is ess
196 cation of LTB4 as a highly potent ligand for BK channels is critical for the future development of be
198 voltage-dependent gating and pore opening in BK channels is modulated to a great extent by the intera
201 ductance voltage- and Ca(2+)-activated K(+) (BK) channel is an important determinant of vascular tone
202 a-specific subtype of Ca(2+)-activated K(+) (BK) channel is responsible for generation of MIH and ant
203 ge-activated potassium channel, known as the BK channel, is one of the central proteins that mediate
204 rge-conductance calcium-activated potassium (BK) channel lacks a classic intracellular bundle-crossin
206 cluding endothelin-1 (ET-1), inhibit myocyte BK channels, leading to contraction, but mechanisms invo
210 ifying endolysosomes by activating TRPML1 or BK channels may provide therapeutic benefit against late
211 ke repolarization and a persistently reduced BK channel mediated afterhyperpolarization (AHP), repeti
212 st step for designing agents that antagonize BK channel-mediated alcohol actions without perturbing b
215 activities preserved BK-beta1 expression and BK-channel-mediated coronary vasodilation in diabetic mi
216 idence from previous studies indicating that BK channels might play a critical role in habituation.
217 ogether, these results suggest that blocking BK channels mimics the effects of ethanol on GABA releas
218 it effectively interferes with mallotoxin on BK channel modulation via either a direct steric competi
219 ese studies indicate that a loss-of-function BK channel mutation causes ataxia and acts by reducing m
223 tance, calcium-activated potassium channels (BK channels) on the NE of rodent hippocampal neurons.
224 d BK channel open probability via increasing BK channel open frequency, but not through prolonging it
226 on of the BKbeta4 subunit alleviated reduced BK channel open probability via increasing BK channel op
227 nel analyses revealed that FMRP loss reduced BK channel open probability, and this defect was compens
228 alcohol increases both alpha and alphabeta4 BK channel open probability, but only alpha BK develops
229 at large-conductance calcium-activated K(+) (BK) channel open probability was reduced by loss of frag
231 of BK channel-mediated unitary currents, the BK channel opener NS1619 attenuated the effects of METH
232 ndent constitutive openness, we propose that BK channel opening involves structural rearrangement of
234 C. elegans, loss of function in SLO-1, the BK channel ortholog, confers profound ethanol resistance
236 de convincing evidence for a crucial role of BK channel phosphorylation in synaptic depression underl
238 ce calcium- and voltage-activated potassium (BK) channels play an important role in generating functi
239 uctance, Ca(2+)- and voltage-dependent K(+) (BK) channels play an important role in this process.
240 analysis of the interaction of PAX with the BK channel pore gate domain guided by recently available
241 eins, of the intracellular S0-S1 loop of the BK channel pore-forming alpha-subunit controls functiona
243 molecular events downstream of cGMP involve BK channels present in cardiomyocytes or in other cardia
249 n of wild-type versions of the worm or human BK channel rescued intoxication and other BK channel-dep
250 n human brain, 2) coexpression of LINGO1 and BK channels resulted in rapidly inactivating BK currents
252 the selectivity filter, we propose that the BK channel's normal closing may represent an early confo
254 worm T381I or equivalent human T352I mutant BK channel selectively rescued BK channel-dependent beha
256 ent kinetic properties, with fast-activating BK channels serving to short-circuit activation of Kv2 c
257 experiments showed that loss of Ca(2+) spark-BK channel signaling in Mcoln1 (-/-) mice rendered both
258 We identified the Caenorhabditis elegans BK channel SLO-1 as a molecular target of the Mel recept
259 does not alter the expression of either the BK channel SLO-1 or the Shaker type potassium channel SH
260 bditis elegans, mutations that eliminate the BK channel, SLO-1, convey dramatic resistance to intoxic
261 LS3 suppresses locomotor activity via a BK channel-specific mechanism in wild-type or BK channel
262 th large-conductance calcium-activated K(+) (BK) channels, specifically their auxiliary beta4 subunit
263 channels were co-expressed in the same cell, BK channels started activating near -50 mV, 30 mV more n
264 0 mM) modify Ca(2+)- and voltage-gated K(+) (BK) channel steady-state activity, eventually altering b
268 ual role: they both support release and fuel BK channels, suggesting that at immature stages presynap
269 y blockade of either SK or BK channels, with BK channels supporting faster synaptic waveforms and SK
270 canonical Wnt/beta-catenin pathway regulates BK channel surface expression in a protein synthesis-dep
272 the S-acylated S0-S1 domain conserved in all BK channels that controls membrane trafficking and is de
273 regulatory subunits, beta and gamma, define BK channels that span a diverse range of functional prop
274 big-conductance Ca(2+)-activated potassium (BK) channels that form physical and functional coupling
276 duration by changing alternative splicing of BK channels; this requires nuclear export of the splicin
277 subunit of the calcium-activated potassium (BK) channel; this interaction increases calcium-dependen
278 st that Mel promotes sleep by activating the BK channel through a specific Mel receptor and Gbetalamb
279 results strongly suggest that AT1R regulates BK channels through a close protein-protein interaction
283 Our study thus indicates that the control of BK channel trafficking is a critical regulatory mechanis
284 and large conductance Ca(2+)-activated K(+) (BK) channels (U251 cells), resulted in time-dependent in
286 resent the external architectural details of BK channels using lanthanide-based resonance energy tran
289 down did not alter Ca(2+) sparks but reduced BK channel voltage sensitivity, which decreased channel
291 n of the Ca(2+)- and voltage-activated K(+) (BK) channel was identified in morbidly obese men carryin
292 tential sites of interaction of PAX with the BK channel, we undertook a computational analysis of the
293 conformational changes in BK-type potassium (BK) channels, we examined consequences of Cd(2+) coordin
294 iated by large conductance, Ca(2+)-activated BK channels, were reduced by nearly 80% (P<0.01) and 25%
295 esults suggest that LINGO1 is a regulator of BK channels, which causes a "functional knockdown" of th
296 e in a BK complex therefore allow a range of BK channels with distinct functional properties tuned by
297 plitude of eIPSCs, whereas the activation of BK channels with the channel opener NS1619 reversibly at
299 OHCs is altered by blockade of either SK or BK channels, with BK channels supporting faster synaptic
300 sites resulted in constitutively open mutant BK channels, with high open probability at negative volt