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1 noylaminoethyl methanethiosulfonate) to show ATP-sensitive accessibility of cysteine mutants at the h
2 d to at least three different channel types: ATP-sensitive, Ca(2+)-regulated and voltage-dependent K(
3 on of GIP, GLP-1 and PYY was sensitive to K+(ATP)-sensitive channel modulators tolbutamide and diazox
6 e that the variant-based channel can form an ATP-sensitive conductance and may contribute to cardiopr
9 RNA-mediated knockdown of ROMK inhibits the ATP-sensitive, diazoxide-activated component of mitochon
12 ization and vasorelaxation by activating the ATP-sensitive, intermediate conductance and small conduc
13 ports that chloroquine inhibition of cardiac ATP-sensitive inward rectifier K(+) current (I(KATP)) is
14 sing on membrane proteins, we identified the ATP-sensitive inward rectifying potassium channel KIR4.1
15 tion of the bee antiviral immune response by ATP-sensitive inwardly rectifying potassium (KATP) chann
16 < 0.05; 0.03 < P(a) < 0.08), as well as with ATP-sensitive inwardly rectifying potassium channel subu
19 strated that opening adenosine triphosphate (ATP)-sensitive K (KATP) channels or activation of delta-
20 up, which binds to adenosine triphosphatase (ATP)-sensitive K(+) (K(ATP)) channels for insulin secret
21 tric oxide (NO), and adenosine triphosphate (ATP)-sensitive K(+) (K(ATP)) channels in adenosine-induc
23 dent I(Ca,L) inactivation, combined with the ATP-sensitive K current agonist pinacidil or I(Ca,L) blo
25 prescribed for diabetes, inhibit pancreatic ATP-sensitive K(+) (K(ATP) ) channels to increase insuli
29 Mutations in the pore-forming subunit of the ATP-sensitive K(+) (K(ATP)) channel Kir6.2 cause neonata
36 on, with particular attention to the role of ATP-sensitive K(+) (K(ATP)) channels and the exact site
41 and the subsequent activation of SUR1/Kir6.2 ATP-sensitive K(+) (K(ATP)) channels inhibit hepatic glu
46 ts evoked by NMDA are greatly potentiated by ATP-sensitive K(+) (K-ATP) channel blocking agents in ST
47 transmitter release by activating inhibitory ATP-sensitive K(+) (KATP ) channels, as well as a class
49 lfonylurea receptor 2 (SUR2) subunits of the ATP-sensitive K(+) (KATP) channel as well as two mutatio
50 The opening of sarcolemmal and mitochondrial ATP-sensitive K(+) (KATP) channels in the heart is belie
51 ptide secretion also required the closing of ATP-sensitive K(+) (KATP) channels, as the KATP channel
52 report a novel target of the drug memantine, ATP-sensitive K(+) (KATP) channels, potentially relevant
54 Ba(2+)) nor inhibitors of the mitochondrial ATP-sensitive K(+) channel (5-hydroxydecanoate and glibe
56 cate that this defect lies downstream of the ATP-sensitive K(+) channel (K(ATP) channel) and calcium
58 with inactivating mutations of the beta-cell ATP-sensitive K(+) channel (K(ATP) channel) genes ABCC8
59 he E23K variant in the Kir6.2 subunit of the ATP-sensitive K(+) channel (K(ATP) channel) is associate
60 determine whether closure of the alpha-cell ATP-sensitive K(+) channel (K(ATP) channel) is the mecha
61 eas and most commonly results from recessive ATP-sensitive K(+) channel (K(ATP) channel) mutations.
62 associated with decreased expression of the ATP-sensitive K(+) channel (K(ATP) channel) sulfonylurea
64 ne (KCNJ11), the pore-forming subunit of the ATP-sensitive K(+) channel (K(ATP) channel), are a commo
65 ne (KCNJ11), the pore-forming subunit of the ATP-sensitive K(+) channel (K(ATP) channel), cause neona
71 ial inhibition of insulin secretion with the ATP-sensitive K(+) channel agonist (opener) diazoxide, c
73 e Kir6.2 and SUR1 subunits of the pancreatic ATP-sensitive K(+) channel are the most common cause of
74 ility transition pore, and the mitochondrial ATP-sensitive K(+) channel did not change the NADH effec
75 from diagnosis and were diagnosed later than ATP-sensitive K(+) channel mutation carriers (11 vs. 8 w
76 ts of the ruthenium complexes suggested that ATP-sensitive K(+) channel pathways were not involved be
77 perpolarization, indicating activation of an ATP-sensitive K(+) channel via a PI3 kinase-dependent me
79 ember 6.2), which encode the subunits of the ATP-sensitive K(+) channel, and RNA in situ hybridizatio
82 s are uncertain but may involve cell surface ATP-sensitive K(+) channels (K(ATP) channels) analogous
86 We also examined the role of hypothalamic ATP-sensitive K(+) channels (K(ATP) channels) in the eff
87 es to hypoglycemia through the modulation of ATP-sensitive K(+) channels (K(ATP) channels) in the ven
89 cytoplasmic [ATP]/[ADP], causing closure of ATP-sensitive K(+) channels (K(ATP) channels), Ca(2+) en
90 sulfonylurea receptor, the stress-responsive ATP-sensitive K(+) channels (K(ATP) channels), with thei
93 e the cAMP-dependent inhibition of beta-cell ATP-sensitive K(+) channels (K(ATP)) was provided by one
96 the effect, indicating that H2S acts through ATP-sensitive K(+) channels and nitric oxide synthesis.
97 ilation was insensitive to the inhibitors of ATP-sensitive K(+) channels and voltage-gated K(+) chann
101 elected mutant, we examine the regulation of ATP-sensitive K(+) channels via a G(q/11)-coupled recept
103 tly coupled to the activation of sarcolemmal ATP-sensitive K(+) channels, hastening action potential
104 generated from glucose is assumed to inhibit ATP-sensitive K(+) channels, leading to the depolarizati
105 mitochondrial proteins such as mitochondrial ATP-sensitive K(+) channels, the mitochondrial permeabil
107 current, a Ca(2+)-activated K(+) current, an ATP-sensitive K(+) current, a plasma membrane calcium-pu
108 ed by oxidative stress activates sarcolemmal ATP-sensitive K(+) currents to form a metabolic sink.
111 variable that controls insulin secretion by ATP-sensitive K(+)-dependent and -independent mechanisms
115 racellular Ca2+, phospholipase A2 (PLA2) and ATP-sensitive K+ (KATP) channel activation whereas A2A-m
117 ften caused by inactivating mutations of the ATP-sensitive K+ (KATP) channel in the pancreatic beta c
120 f the JCI, Oduori et al. explore the role of ATP-sensitive K+ (KATP) channels in maintaining glucose
121 the sulfonylurea glibenclamide, implicating ATP-sensitive K+ (KATP) channels; however, tissue ATP wa
122 were examined on membrane potential and the ATP-sensitive K+ channel (K ATP) in INS 832/13 cells.
123 ion on chromosome 6q24, and 14 patients with ATP-sensitive K+ channel (K(ATP) channel) gene mutations
126 ardioprotective signal and the mitochondrial ATP-sensitive K+ channel (mitoK(ATP)) plays a crucial ro
127 rmacological modulation of the mitochondrial ATP-sensitive K+ channel (mitoKATP) sensitive to diazoxi
128 ts were reversed by a specific mitochondrial ATP-sensitive K+ channel inhibitor, 5-hydroxydecanoate,
129 ectifier subunits Kir 6.1 and Kir 6.2 of the ATP-sensitive K+ channel of the plasma membrane (cellKAT
130 arious types of cells with the mitochondrial ATP-sensitive K+ channel opener, diazoxide, precondition
131 show that tolbutamide, an antagonist of the ATP-sensitive K+ channel, allows these oscillations to t
134 via Epac1 and/or Epac2 to inhibit beta-cell ATP-sensitive K+ channels (K(ATP) channels; a hetero-oct
135 iding novel insight into the architecture of ATP-sensitive K+ channels (KATP channels) (KIR6.0/SUR)4.
138 nty years after the discovery of sarcolemmal ATP-sensitive K+ channels and 12 years after the discove
141 d glucose trigger insulin release by closing ATP-sensitive K+ channels, depolarizing beta cells, and
143 een the degree of coupling and the extent of ATP-sensitive K+-channel activation and illustrates an e
152 viously shown that Ca(2+) directly activates ATP-sensitive microtubule binding by a Chlamydomonas out
154 ated pressor response, and (2) activation of ATP-sensitive P2X receptors enhances the pressor respons
158 by the putative blocker of the mitochondrial ATP sensitive potassium channel, 5-hydroxydecanoate, bef
161 ), and the selective adenosine triphosphate (ATP)-sensitive potassium (K(ATP)) channel blocker gliben
162 rming subunit of the adenosine triphosphate (ATP)-sensitive potassium (KATP) channel, cause neonatal
166 signaling in POMC neurons that elevates the ATP-sensitive potassium (K(ATP)) channel activity cell-a
167 resent investigation we examined the role of ATP-sensitive potassium (K(ATP)) channel activity in mod
169 responding to cytoplasmic nucleotide levels, ATP-sensitive potassium (K(ATP)) channel activity provid
170 loss of function mutations of the beta-cell ATP-sensitive potassium (K(ATP)) channel can develop hyp
174 Furthermore, leptin indirectly activated an ATP-sensitive potassium (K(ATP)) channel in OX neurons,
176 nitric oxide (NO) donor nitroprusside or the ATP-sensitive potassium (K(ATP)) channel opener cromakal
179 tivating mutations in the genes encoding the ATP-sensitive potassium (K(ATP)) channel subunits Kir6.2
180 irpin RNA (shRNA) inhibited the hypothalamic ATP-sensitive potassium (K(ATP)) channel with glibenclam
184 ding Kir6.2, the pore-forming subunit of the ATP-sensitive potassium (K(ATP)) channel, are the most c
185 odes Kir6.2, the pore-forming subunit of the ATP-sensitive potassium (K(ATP)) channel, cause permanen
187 r6.2 pore-forming subunit of the sarcolemmal ATP-sensitive potassium (K(ATP)) channel, predisposed to
188 el Kir6.2 is the pore-forming subunit of the ATP-sensitive potassium (K(ATP)) channel, which controls
189 d the mechanism of chloroquine inhibition of ATP-sensitive potassium (K(ATP)) channels (Kir6.2/SUR2A)
191 ng gated by high-energy nucleotides, cardiac ATP-sensitive potassium (K(ATP)) channels are exquisitel
199 conducted to examine the role of myocardial ATP-sensitive potassium (K(ATP)) channels in exercise-in
200 ulation of EGP by activation of hypothalamic ATP-sensitive potassium (K(ATP)) channels in rodents, wh
207 requires high-fidelity metabolic sensing by ATP-sensitive potassium (K(ATP)) channels that adjust me
208 les with sulfonylurea receptor 1 to form the ATP-sensitive potassium (K(ATP)) channels that regulate
209 mate via H(2)O(2) signaling, which activates ATP-sensitive potassium (K(ATP)) channels to inhibit dop
211 (ROS), coupled to the opening of sarcolemmal ATP-sensitive potassium (K(ATP)) channels, contributes t
213 ely 70% of the beta-cells have nonfunctional ATP-sensitive potassium (K(ATP)) channels, whereas the r
216 e decrease in SNr firing was not mediated by ATP-sensitive potassium (KATP) channel activity, but if
217 ess, the ATP/ADP ratio increases, leading to ATP-sensitive potassium (KATP) channel closure, which in
219 sulphonylurea receptor (SUR1) subunit of the ATP-sensitive potassium (KATP) channel is a member of th
222 that Epac exists in a complex with vascular ATP-sensitive potassium (KATP) channel subunits and that
223 mutation, W68R, in the Kir6.2 subunit of the ATP-sensitive potassium (KATP) channel, in a patient wit
224 ggering of insulin secretion mediated by the ATP-sensitive potassium (KATP) channel, was decreased in
228 carbamazepine, correct biogenesis defects in ATP-sensitive potassium (KATP) channels composed of sulf
233 In the absence of intracellular nucleotides, ATP-sensitive potassium (KATP) channels exhibit spontane
234 while simultaneously recording currents from ATP-sensitive potassium (KATP) channels in single cells,
235 r 2B (SUR2B) forms the regulatory subunit of ATP-sensitive potassium (KATP) channels in vascular smoo
237 (NO) synthase, soluble guanylyl cyclase, and ATP-sensitive potassium (KATP) channels nearly abolished
240 sarcolemmal (sarc) and mitochondrial (mito) ATP-sensitive potassium (KATP) channels play crucial rol
242 Insulin secretion is under the control of ATP-sensitive potassium (KATP) channels that play key ro
245 nes encoding the Kir6.1 and SUR2 subunits of ATP-sensitive potassium (KATP) channels, respectively.
248 by leptin mirror those reported recently for ATP-sensitive potassium (KATP) channels, which are criti
250 acking the Kir6.2 subunit of the sarcolemmal ATP-sensitive potassium (sK(ATP)) channel after exposure
253 a protein that combines with SUR2 to form an ATP-sensitive potassium channel (K(ATP)) expressed in co
257 odes Kir6.2, the pore-forming subunit of the ATP-sensitive potassium channel (K(ATP)), are the common
258 e perfused with Ringer solution (control), a ATP-sensitive potassium channel (KATP ) inhibitor, an in
260 ells were compared to those of the reference ATP-sensitive potassium channel (KATP channel) openers d
261 ; encoded by ABCC8) and its associated islet ATP-sensitive potassium channel (Kir6.2; encoded by KCNJ
263 conditioning with diazoxide, a mitochondrial ATP-sensitive potassium channel agonist, prevented dendr
264 wnstream glucokinase effectors revealed that ATP-sensitive potassium channel and P/Q calcium channel
265 eir supramolecular assemblies, including the ATP-sensitive potassium channel and the peptide-loading
266 h DZX, supporting a role for a mitochondrial ATP-sensitive potassium channel in the mechanism of card
267 isolation buffer, cardioplegia (CPG)+/-DZX+/-ATP-sensitive potassium channel inhibitor, 5-hydroxydeca
269 response to stress that is prevented by the ATP-sensitive potassium channel opener, diazoxide (DZX)
270 by covalently modifying (sulfhydrating) the ATP-sensitive potassium channel, as mutating the site of
271 ein kinase G-inhibitor) or glibenclamide (an ATP-sensitive potassium channel-inhibitor) all led to an
283 is the prototypical opener of mitochondrial ATP-sensitive potassium channels (mitoK(ATP)) and protec
284 we demonstrated that targeting mitochondrial ATP-sensitive potassium channels (mitoK(ATP)) protects n
285 lucose cotransporter SGLT1, or by closure of ATP-sensitive potassium channels after glucose metabolis
286 gers membrane depolarization both by closing ATP-sensitive potassium channels and because of its upta
287 version to lactate, leading to activation of ATP-sensitive potassium channels and to decreased hepati
288 nhibitor), 5-hydroxydecanoate (mitochondrial ATP-sensitive potassium channels inhibitor), or glibencl
289 tassium channel (Ir), proteins that comprise ATP-sensitive potassium channels regulating hormone secr
290 and unclear and may involve Akt activation, ATP-sensitive potassium channels, and nitric oxide, amon
296 e composition and signaling of an endogenous ATP-sensitive potassium ion channel (KATP) in HepG2C3A,
298 malian SUR genes are associated with K(ATP) (ATP-sensitive potassium) channels, which are involved in
299 SGs assembled by stem-loop RNA triggers are ATP-sensitive, regulated by helicase/chaperone activity,
300 s been proposed as a regulator of the 30 pS, ATP-sensitive renal K channel (Kir1.1, also known as ren