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1 onductance SK channels and large-conductance BK channels).
2 ion permeation gate at the cytosolic side of BK channel.
3  effect of beta4 on kinase modulation of the BK channel.
4 lectively disrupts ethanol modulation of the BK channel.
5  to a well-characterized pore blocker of the BK channel.
6 ncreases calcium-dependent activation of the BK channel.
7 g the pore of heterologously expressed human BK channels.
8 isengagement of the gamma1-F273S mutant from BK channels.
9 blished, little is known about how they open BK channels.
10 y of recombinant and prostate adenocarcinoma BK channels.
11  understand the tissue-specific functions of BK channels.
12 chanisms controls cell surface expression of BK channels.
13  are thought to be ineffective at activating BK channels.
14 unction as LRRC26-type auxiliary subunits of BK channels.
15 s display discrete substrate specificity for BK channels.
16 hydroabietic acid derivative Cym04 activates BK channels.
17 y a small effect on the action of NS-1619 on BK channels.
18  close apposition of ryanodine receptors and BK channels.
19 ls, which in turn are specifically linked to BK channels.
20 uctance, voltage- and Ca(2+)-activated K(+) (BK) channels.
21 gy of large conductance calcium-activated K (BK) channels.
22 a(2+)-activated, and voltage dependent K(+) (BK) channels.
23  the activity of Ca(2+)-activated potassium (BK) channels.
24  the activity of Ca(2+)-activated potassium (BK) channels.
25                                       In the BK channel, a large C-terminal intracellular region cont
26  an example from fish showing that increased BK channel abundance can improve an individual's ability
27  cortical/medullary collecting duct, whereas BK channel abundance increased in principal cells of the
28 mSlo1 and further developed a model in which BK channels act as a calcium sensor capable of quantitat
29 n mallotoxin and the gamma subunits in their BK channel-activating effects in membrane patches excise
30 oteolysis, leading to the down-regulation of BK channel activation and impaired coronary function in
31                                 We show that BK channel activation and subsequent phosphorylation of
32 angement allows tight tracking between local BK channel activation and the gating of CaV1.3 channels
33                                              BK channel activation depends on the interactions among
34                  How beta subunits fine-tune BK channel activation is critical to understand the tiss
35                      Our study suggests that BK channel activation stimulates the TRPML1-BK positive
36 chanism by which the beta subunits modulated BK channel activation such that a beta subunit may inter
37 lic acid (LCA) dilates cerebral arteries via BK channel activation, which requires recognition by a B
38 on via a fast afterhyperpolarization through BK channel activation.
39        Mallotoxin is a potent small-molecule BK channel activator.
40 for the future development of beta1-specific BK channel activators.
41 llosterically coupled to each other, control BK channel activity and are potential targets for regula
42                             We conclude that BK channel activity directly affects vascular tone but i
43  determine the significance of smooth muscle BK channel activity for blood pressure regulation, we in
44 unit surface trafficking controls functional BK channel activity in arterial myocytes and vascular co
45                          Rottlerin increased BK channel activity in human ASM cells (V50 shifted by 7
46 dulation, allowing a variety of outcomes for BK channel activity in response to acute alcohol.
47 nockout (dKO) mice to genetically upregulate BK channel activity in the absence of FMRP and determine
48 ice were generated to genetically upregulate BK channel activity in the absence of FMRP.
49                                              BK channel activity is tightly regulated by its accessor
50 C mice, implying that impaired smooth muscle BK channel activity lowers blood pressure in these anima
51 ur studies thus suggest that upregulation of BK channel activity normalizes multi-level deficits caus
52                      Genetic upregulation of BK channel activity via deletion of BKbeta4 normalized a
53                      Genetic upregulation of BK channel activity via deletion of BKbeta4 was sufficie
54 onses is, in part, due to METH regulation of BK channel activity.
55 voltage- and Ca(2+)-sensitive K(+) channels (BK channels) after action potentials, and random activat
56 onstrate that systemic administration of the BK channel agonist rottlerin (5 mug/g) during the challe
57 vel large-conductance Ca(2+)-activated K(+) (BK) channel agonist that shifts the activation V1/2 of t
58 ysosomal storage diseases (LSDs) and whether BK channel agonists rescue abnormal lysosomal storage in
59 arge-conductance Ca(2+)-activated potassium (BK) channel alpha and auxiliary beta1 subunits that are
60 m channels), recent findings have shown that BK channels also contribute to inhibition in basal, high
61                    Cholesterol modulation of BK channels alters action potential firing, colonic ion
62  role of MuRF1 in the regulation of vascular BK channel and coronary function has not been examined.
63 tion, surface trafficking of beta1 subunits, BK channel and transient BK current activation, and vaso
64 ced reduction of whole cell BK currents, and BK channels and ANG-II receptors were found to co-locali
65 ed in dietary supplements, fails to activate BK channels and antagonizes the stimulatory effect of DH
66 e voltage gating of heterologously expressed BK channels and causes a dramatic increase in the activi
67 flash photolysis of caged Ca(2+) to activate BK channels and determine their intrinsic sensitivity to
68 scillations sufficiently to activate endfoot BK channels and elevate [K(+)](o) in the restricted peri
69 ite to selectively activate beta1-containing BK channels and evoke vasodilation remain unknown.
70 s of CaV1.3 channels surrounding clusters of BK channels and forming a multi-channel complex both in
71 -frequency (apical) OHCs that do not express BK channels and from immature high-frequency OHCs before
72 echanism by which a vasoconstrictor inhibits BK channels and identify Rab11A serine 177 as a modulato
73 mary mechanism by which NO activates myocyte BK channels and induces vasodilation.
74            We induced C-type inactivation in BK channels and studied the relationship between activat
75                        ET-1 inhibited single BK channels and transient BK currents in myocytes and st
76 rge-conductance calcium-activated potassium (BK) channels and Kv3.3 voltage-gated potassium channels
77 ), voltage- and calcium-activated potassium (BK) channels and their modulatory beta-subunits are able
78 alling pathways such as K(+) release through BK channels, and the production and release of arachidon
79 rge-conductance calcium-activated potassium (BK) channels, and this effect is mediated through the cA
80       Blocking BK channels with the specific BK channel antagonist paxilline significantly increased
81 eases in mIPSC frequency by either selective BK channel antagonists or ethanol were not accompanied w
82 ltage clamp, and their response to selective BK channel antagonists, channel activators, or ethanol w
83 corded from high-frequency OHCs that express BK channels are briefer than IPSCs recorded from low-fre
84      In the first cluster, T-type Ca(2+) and BK channels are coupled within distances of ~20 nm (200
85 e-conductance Ca(2+)- and voltage-gated Slo1 BK channels are directly activated by nanomolar levels o
86 pendent stimulation by DHA demonstrates that BK channels are effectors of omega-3 fatty acids with ma
87 der high-calorie conditions, suggesting that BK channels are promising drug targets for pharmacothera
88                      Because depalmitoylated BK channels are retarded in the trans-Golgi network, rev
89                    Our results indicate that BK channels are strongly modulated by activation of spec
90                                         Slo1 BK channels are thus receptors for long-chain omega-3 fa
91 arge-conductance calcium-activated potassium BK channels are widely expressed in the brain and are in
92 big conductance calcium-activated potassium (BK) channel are preferentially expressed by electrosenso
93         Large conductance calcium-activated (BK) channels are broadly expressed in neurons and muscle
94 ance, voltage-, and Ca(2)(+)-dependent K(+) (BK) channels are broadly expressed in various tissues to
95 ctance calcium (Ca)(2+)-activated potassium (BK) channels are functionally significant modulators of
96 ce voltage- and calcium-activated potassium (BK) channels are highly expressed in airway smooth muscl
97 ductance Ca(2+)- and voltage-activated K(+) (BK) channels are involved in a large variety of physiolo
98 uctance voltage- and calcium-activated K(+) (BK) channels are key physiological players in muscle, ne
99 ductance voltage- and Ca(2+)-activated K(+) (BK) channels are potent regulators of cellular processes
100 ductance Ca(2+)- and voltage-activated K(+) (BK) channels are well known for their functional versati
101 dependent and calcium-activated K(+) (MaxiK, BK) channels are widely expressed in many tissues and or
102                                 Furthermore, BK channels as well as purinergic receptors were shown t
103                                    Silencing BK channel auxiliary beta3 subunit significantly attenua
104 d we designate them as a gamma family of the BK channel auxiliary proteins, which potentially regulat
105 R)-containing membrane protein, LRRC26, as a BK channel auxiliary subunit, which causes an unpreceden
106 Ca(2+)/voltage-gated K(+) large conductance (BK) channel beta1 subunit is particularly abundant in va
107 eted mouse model with global ablation of the BK channel (BK(L1/L1)) and adipocyte-specific BK-deficie
108 r voltage dependence and their response to a BK channel blocker or opener.
109   Furthermore, following bath application of BK channel blockers for 10 min, ethanol failed to furthe
110                   Bath application of either BK channel blockers significantly increased the frequenc
111  spike frequency, a mechanism independent of BK channels but dependent on background non-selective co
112  spike frequency, a mechanism independent of BK channels but dependent on background non-selective co
113   In arterial smooth muscle, ANG-II inhibits BK channels, but the underlying molecular mechanisms are
114 iary gamma1-3 subunits potently modulate the BK channel by shifting its voltage-dependence of channel
115       Test the hypothesis that ET-1 inhibits BK channels by altering BKalpha and beta1 surface traffi
116 ominent slow C-type inactivation/recovery in BK channels by an extreme low concentration of extracell
117 gest METH exposure decreased the activity of BK channels by decreasing BK-alpha subunit levels at the
118 veal an all-or-none functional regulation of BK channels by gamma-subunits: channels either exhibit a
119 nd thus may contribute to the suppression of BK channels by mAChRs.
120 rdation protein (FMRP) and that FMRP acts on BK channels by modulating the channel's gating kinetics.
121 We found that METH decreased the activity of BK channels by stimulating BK-alpha subunit trafficking.
122  that selectively activates beta1-containing BK channels by targeting the steroid-sensing site in BK
123 ted large conductance Ca(2+)-activated K(+) (BK) channel by associated gamma1-subunits.
124                            We concluded that BK channel C-type inactivation is closed state-dependent
125                   However, we found that the BK channel C-type inactivation occurred during hyperpola
126 rface beta1 subunits leads to a reduction in BK channel calcium-sensitivity, inhibition of transient
127 t cations sensed by a large structure in the BK channel called the "gating ring," which is formed by
128 the cells with blockers of either the NSC or BK channels, caused a strong inhibition of the A23187-in
129 rom the trans-Golgi network and thus control BK channel cell surface expression.
130              By measuring gating currents in BK channels coexpressed with chimeras between beta1 and
131 tely 500 nM rapidly and reversibly activates BK channels composed of the pore-forming Slo1 subunit an
132 uctance, calcium- and voltage-activated K(+)(BK) channel consists of the pore-forming alpha subunits
133       Together, these findings indicate that BK channels contribute to postsynaptic function, and inf
134                Therefore, microglia-specific BK channels contribute to the generation of MIH and anti
135 /voltage-gated, large conductance potassium (BK) channels control numerous physiological processes, i
136 ethanol on GABA release and that presynaptic BK channels could serve as a target for ethanol effects
137         The molecular mechanisms of AT1R and BK channel coupling were investigated in co-transfected
138 AL-8810 (FP receptor antagonist)-insensitive BK channel currents with EC(50)s of 0.51 +/- 0.03 nM (n
139 ely 30% identity to APT1, that also controls BK channel depalmitoylation.
140 an BK channel rescued intoxication and other BK channel-dependent behaviors in a slo-1-null mutant ba
141  T352I mutant BK channel selectively rescued BK channel-dependent behaviors while conveying resistanc
142   This mutation did not interfere with other BK channel-dependent behaviors, suggesting that the muta
143      We here identify, for the first time, a BK channel-dependent molecular synaptic mechanism leadin
144 e of the mechanisms responsible for creating BK channel diversity fundamental to the adequate functio
145                               We reveal that BK channels do not play a significant role in the genera
146                               We reveal that BK channels do not play a significant role in the genera
147 BK-beta(1) degradation and leads to diabetic BK channel dysfunction.
148 ch-clamp recordings confirmed that the human BK channel engineered with the T352I missense mutation w
149 The large conductance Ca(2+)-activated K(+) (BK) channel, expressed abundantly in vascular smooth mus
150 istent with the importance of a reduction in BK channel expression and function in mediating the HF-i
151 ng that NDO is associated with decreased DSM BK channel expression and function leading to increased
152 rect upregulation of ENaC, whereas increased BK channel expression has a less significant role.
153 for BK channels, viral-mediated increases in BK channel expression in SCA1 Purkinje neurons improves
154 uency OHCs before the developmental onset of BK channel expression.
155 SM) large conductance Ca(2+)-activated K(+) (BK) channel expression and function.
156 studies in Xenopus oocytes that co-expressed BK channel-forming (cbv1) and accessory beta1 subunits c
157 e, we demonstrate that cholesterol action on BK channel-forming Cbv1 proteins is mediated by their cy
158  big conductance Ca(2+)-activated potassium (BK) channel forms a physical and functional coupling wit
159 2+)]i Constitutively open mutation prevented BK channels from C-type inactivation.
160 e protein, promotes the trafficking of SLO-1 BK channels from the ER to the plasma membrane by shield
161 ght the importance of not only CFTR but also BK channel function in maintaining ASL homeostasis and e
162                                     However, BK channel function is impaired in diabetic vessels by i
163                       Minimal alterations in BK channel function may contribute to the pathophysiolog
164 a on aldosterone regulation by renal/adrenal BK channel function, BKbeta1(-/-) strain A mice have inc
165 ownregulates CFTR activity but also inhibits BK channel function, thereby causing ASL depletion.
166 n pharmaceutical applications for modulating BK channel function.
167 yer of complexity to the mechanisms by which BK channel functional diversity is generated.
168  that arterial myocytes express a functional BK channel gamma subunit.
169                        BK channel openers or BK channel gene transfer could be an alternative strateg
170                            Inhibiting Kv2 or BK channels had very different effects on spike shape an
171 ce lacking the pore-forming alpha-subunit of BK channels have longer IPSCs than do the OHCs of BKalph
172 nductance voltage and Ca(2+)-activated K(+) (BK) channel have a key role in the ethanol effect on GPe
173                         We record from human BK channels heterologously expressed in HEK 293 cells co
174 K channel-specific mechanism in wild-type or BK channel-humanized Caenorhabditis elegans.
175 ermined (i) a basic extracellular map of the BK channel, (ii) beta1-subunit-induced rearrangements of
176 ed role for glucocorticoids in regulation of BK channels in airway epithelial cells.
177                         First, we identified BK channels in dopamine neurons by their voltage depende
178 auses a dramatic increase in the activity of BK channels in human smooth muscle cells.
179                      We assessed the role of BK channels in modulating the action of ethanol on inhib
180  In summary, we demonstrate a novel role for BK channels in regulating glutamatergic transmission and
181 s leads to the sole activation of microglial BK channels in the spinal cord.
182          Furthermore, positive modulation of BK channels in vivo can enhance short-term habituation.
183 ce calcium- and voltage-activated potassium (BK) channels in spontaneous and secretagogue-induced act
184  conductance calcium- and voltage-activated (BK) channels in spontaneous and secretagogue-induced act
185  of large-conductance Ca(2+)-activated K(+) (BK) channels in the nervous system has been extensively
186                                              BK channel inhibition by PKC, however, was effectively e
187 requency-current (f-I) relationship, whereas BK channel inhibition had little effect on the f-I slope
188 ased sensitivity to iberiotoxin, a selective BK channel inhibitor, in DSM strips isolated from NDO pa
189 n to iberiotoxin and vasodilation to NS1619, BK channel inhibitors and activators, respectively.
190 effect on GPe neurons, as the application of BK channel inhibitors blocked the ethanol-induced firing
191          Site(s) and mechanism(s) of ethanol-BK channel interaction are unknown.
192  The structural bases underlying cholesterol-BK channel interaction are unknown.
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
195          CaV-channel dependent activation of BK channels is critical for feedback control of both cal
196 cation of LTB4 as a highly potent ligand for BK channels is critical for the future development of be
197 s of regulatory proteins, beta and gamma, in BK channels is exclusive or independent.
198               Activation of Ca(2+)-dependent BK channels is increased via binding of micromolar Ca(2+
199                      One potent activator of BK channels is mallotoxin (MTX), which produces a very l
200                      The open probability of BK channels is regulated by the intracellular concentrat
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 effect on steady-state activation of parotid BK channels, it produced an approximate 2-fold speeding
204  Ca(2+)- and voltage-activated K(+) (Slo1 or BK) channels (KCNMA1) play key roles in many physiologic
205 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
207                                              BK channels localize in the cilia of surface cells.
208  lower blood pressure by activating vascular BK channels made of Slo1+beta1 subunits.
209 ke repolarization and a persistently reduced BK channel mediated afterhyperpolarization (AHP), repeti
210 st step for designing agents that antagonize BK channel-mediated alcohol actions without perturbing b
211 r) reduced atrogin-1 expression and restored BK channel-mediated coronary vasodilation in diabetic mi
212       While METH suppressed the amplitude of BK channel-mediated unitary currents, the BK channel ope
213 s reduced BK-beta1 expression and diminished BK channel-mediated vasodilation.
214 activities preserved BK-beta1 expression and BK-channel-mediated coronary vasodilation in diabetic mi
215 idence from previous studies indicating that BK channels might play a critical role in habituation.
216 ogether, these results suggest that blocking BK channels mimics the effects of ethanol on GABA releas
217              These findings demonstrate that BK channels modulate visual responses in vivo at the bip
218 it effectively interferes with mallotoxin on BK channel modulation via either a direct steric competi
219 M samples from NDO patients showed decreased BK channel mRNA expression in comparison to controls.
220            Functionally, blockade of nuclear BK channels (nBK channels) induces NE-derived Ca(2+) rel
221 ild-type mice but are profoundly impaired in BK channel-null mice.
222 tance, calcium-activated potassium channels (BK channels) on the NE of rodent hippocampal neurons.
223 d BK channel open probability via increasing BK channel open frequency, but not through prolonging it
224                       Ethanol also increased BK channel open probability measured in single-channel r
225 on of the BKbeta4 subunit alleviated reduced BK channel open probability via increasing BK channel op
226 nel analyses revealed that FMRP loss reduced BK channel open probability, and this defect was compens
227  alcohol increases both alpha and alphabeta4 BK channel open probability, but only alpha BK develops
228 at large-conductance calcium-activated K(+) (BK) channel open probability was reduced by loss of frag
229                              Addition of the BK channel opener NS11021 directly activated channels in
230 of BK channel-mediated unitary currents, the BK channel opener NS1619 attenuated the effects of METH
231                                              BK channel openers or BK channel gene transfer could be
232 l trials are needed to evaluate the value of BK channel opening drugs or gene therapies for NDO treat
233 ndent constitutive openness, we propose that BK channel opening involves structural rearrangement of
234 stinct sites, voltage sensor activation, and BK channel opening.
235                               Thus, a potent BK channel peptide modulator is open to neurological app
236 de convincing evidence for a crucial role of BK channel phosphorylation in synaptic depression underl
237        In the retina, it has been shown that BK channels play a pivotal role in modulating feedback f
238                  Angiotensin II (ANG-II) and BK channels play important roles in the regulation of bl
239 ce calcium- and voltage-activated potassium (BK) channels play an important role in generating functi
240 uctance, Ca(2+)- and voltage-dependent K(+) (BK) channels play an important role in this process.
241  molecular events downstream of cGMP involve BK channels present in cardiomyocytes or in other cardia
242 conductance, Ca(2+)- and voltage-gated K(+) (BK) channel proteins are ubiquitously expressed in cell
243 ductance Ca(2+)- and voltage-activated K(+) (BK) channels provide a critical vasodilatory influence.
244 ate that IP(3)-mediated activation of SK and BK channels provides a robust mechanism for glutamatergi
245               Voltage- and calcium-dependent BK channels regulate calcium-dependent cellular events s
246                                              BK channel regulation by direct interaction between lipi
247                                     Blocking BK channels relieves voltage-dependent magnesium block o
248                              Drugs targeting BK channel represent a potential therapeutic approach fo
249 n of wild-type versions of the worm or human BK channel rescued intoxication and other BK channel-dep
250                     We hypothesized that the BK channel's activation gate may spatially overlap or co
251  the selectivity filter, we propose that the BK channel's normal closing may represent an early confo
252 cesses this site in presence of calcium, the BK channel's physiological agonist.
253  by BK channels via interaction of FMRP with BK channel's regulatory beta4 subunits.
254 55, and LRRC38 produce a marked shift in the BK channel's voltage dependence of activation in the hyp
255  worm T381I or equivalent human T352I mutant BK channel selectively rescued BK channel-dependent beha
256 nce voltage- and Ca(2+)-activated K(+) (Slo1 BK) channels serve numerous cellular functions, and thei
257 ent kinetic properties, with fast-activating BK channels serving to short-circuit activation of Kv2 c
258  does not alter the expression of either the BK channel SLO-1 or the Shaker type potassium channel SH
259 bditis elegans, mutations that eliminate the BK channel, SLO-1, convey dramatic resistance to intoxic
260      LS3 suppresses locomotor activity via a BK channel-specific mechanism in wild-type or BK channel
261 th large-conductance calcium-activated K(+) (BK) channels, specifically their auxiliary beta4 subunit
262 channels were co-expressed in the same cell, BK channels started activating near -50 mV, 30 mV more
263 0 mM) modify Ca(2+)- and voltage-gated K(+) (BK) channel steady-state activity, eventually altering b
264 tor for measurements of distances within the BK channel structure in a living cell.
265 y blockade of either SK or BK channels, with BK channels supporting faster synaptic waveforms and SK
266 canonical Wnt/beta-catenin pathway regulates BK channel surface expression in a protein synthesis-dep
267                       Here we report a novel BK channel-targeted peptide with functional activity in
268 d the pial cerebral arterioles via selective BK-channel targeting.
269 second cluster consists of L-type Ca(2+) and BK channels that are spread over distances of at least 6
270 ction for FMRP as a regulator of presynaptic BK channels that modulate the dynamics of neurotransmitt
271  big-conductance Ca(2+)-activated potassium (BK) channels that form physical and functional coupling
272 rge-conductance calcium-activated potassium (BK) channels that modulate AP width.
273  subunit of the calcium-activated potassium (BK) channel; this interaction increases calcium-dependen
274 results strongly suggest that AT1R regulates BK channels through a close protein-protein interaction
275 beta4-subunit controls surface expression of BK channels through masking of a trafficking motif in th
276 rmining their phenotype, BK beta1 allows the BK channels to reduce myogenic tone, facilitating vasodi
277 late the multisubunit composition of surface BK channels to stimulate contraction is unclear.
278      Pharmacological manipulations targeting BK channels, together with measures of BK transcript abu
279  affinity is higher than known high affinity BK channel toxins.
280 Our study thus indicates that the control of BK channel trafficking is a critical regulatory mechanis
281 and large conductance Ca(2+)-activated K(+) (BK) channels (U251 cells), resulted in time-dependent in
282 ge-conductance, calcium-activated potassium (BK) channels underlie a primary outward current having a
283                                              BK channel upregulation was also sufficient to correct e
284 resent the external architectural details of BK channels using lanthanide-based resonance energy tran
285  independent and are mediated selectively by BK channels via interaction of FMRP with BK channel's re
286 is drug selectively targets beta1-containing BK channels via the BK beta1 steroid-sensing site.
287               Supporting a critical role for BK channels, viral-mediated increases in BK channel expr
288 down did not alter Ca(2+) sparks but reduced BK channel voltage sensitivity, which decreased channel
289 that the sole AT1R expression could decrease BK channel voltage sensitivity.
290 n of the Ca(2+)- and voltage-activated K(+) (BK) channel was identified in morbidly obese men carryin
291 gly inhibited the ability of MTX to activate BK channels, we found that it had only a small effect on
292 conformational changes in BK-type potassium (BK) channels, we examined consequences of Cd(2+) coordin
293 iated by large conductance, Ca(2+)-activated BK channels, were reduced by nearly 80% (P<0.01) and 25%
294 ational changes of the gating-ring region of BK channels, while simultaneously monitoring channel con
295        Here we examined the action of DHA on BK channels with different auxiliary subunit composition
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
298                                     Blocking BK channels with the specific BK channel antagonist paxi
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

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