コーパス検索結果 (left1)
通し番号をクリックするとPubMedの該当ページを表示します
1 ASIC currents triggered by pH 5 disappeared in the VLM n
2 ASIC proteins can form both homotrimeric and heterotrime
3 ASIC subunits contain intracellular N and C termini, two
4 ASIC-3(+/+) FLS showed enhanced cell death when exposed
5 ASICs (acid-sensing ion channels) are proton-gated chann
6 ASICs are formed as homotrimers or heterotrimers of seve
7 ASICs are involved in fear and anxiety, learning, neurod
8 ASICs have been implicated in several neuronal disorders
9 ASICs represent a widespread communication system with u
10 ASICs undergo steady-state desensitization, a characteri
12 ional homomeric Acid-sensing ion channel-1a (ASIC-1as) that can be activated by protons (coreleased w
13 on nociceptors, acid-sensing ion channel 3 (ASIC-3) is activated by decreases in pH and plays a sign
14 ate that acid-sensing ion channel subtype 3 (ASIC(3)) in thin-fibre muscle afferents contributes to t
15 ions of ASIC1 alone or combined with other 4 ASIC genes are significantly correlated with poor patien
17 ecently showed that decreases in pH activate ASIC-3 located on fibroblast-like synoviocytes (FLS), wh
21 FPI induces cerebral acidosis that activates ASIC channels and contributes to secondary injury in TBI
22 modulate synaptic transmission by activating ASIC-1as at the calyx of Held-MNTB synapse.SIGNIFICANCE
25 of ligands that modulate the function of all ASICs as well as activate ASIC3 at physiological pH.
28 ated the pressor response to lactic acid, an ASIC agonist, but did not attenuate the pressor response
30 90% (9/10) of the labelled neurons showed an ASIC-like response to pH 7.0, suggesting that ASIC curre
32 r of sucrose has been discussed from ASV and ASIC parameters, as these parameters, which are sensitiv
39 vator of ASICs is extracellular protons, and ASICs have been demonstrated to play a significant role
40 nsmembrane helices in both P2X receptors and ASICs, and the method will allow precise optical control
41 hough amiloride has been shown to antagonize ASICs, it also has been shown to antagonize voltage-gate
42 majority of current responses to pH 6.7 are ASIC(3)-like in DRG neurons with nerve endings in the hi
44 ammalian neuronal DEG/ENaC channels known as ASICs (acid-sensing ion channels) mediate sensory percep
45 hat femoral artery occlusion mainly augments ASIC(3) expression within DRG neurons projecting C-fibre
48 eptide psalmotoxin, which profoundly blocked ASIC currents in the hippocampal neurons, had no effect
50 used in our experiments selectively blocked ASICs, whereas the high dose blocked ASICs and impulse c
51 e in NP cells which is inhibited by blocking ASIC-3 activity, suggesting that this may be a useful th
53 amplitude of DRG neuron response induced by ASIC(3) stimulation is larger in occluded rats than that
54 At least some of this current is carried by ASICs because the current is increased by both Zn(2+), a
55 se neuronal activity can produce pH changes, ASICs may respond to local acidic transients and alter t
60 lular pH, leads to acid-sensing ion channel (ASIC) activation and reflexively increases mean arterial
61 s inhibited by the acid-sensing ion channel (ASIC) blocker amiloride, absent in Na+-free bathing solu
62 Other types of acid-sensing ion channel (ASIC) channels were intact to sevanol application, excep
65 channel (ENaC) and acid-sensing ion channel (ASIC) members of the DEG/ENaC superfamily of amiloride-s
66 at a member of the acid-sensing ion channel (ASIC) subfamily of the DEG/ENaC superfamily is an import
98 ation depended on acid-sensing ion channels (ASICs) because treatment of sensory afferents in vitro w
101 via activation of acid-sensing ion channels (ASICs) could have therapeutic application in a host of n
106 PV1) channels and acid-sensing ion channels (ASICs) is that their ion conduction pores dilate upon pr
112 pharmacology with acid-sensing ion channels (ASICs), a small family of excitatory neurotransmitter re
114 ve shown that the acid-sensing ion channels (ASICs), members of the epithelial Na+ channel (ENaC)/deg
115 s for protons are acid-sensing ion channels (ASICs), Na(+)- and Ca(2+)-permeable channels that are ac
117 ctive agonist for acid-sensing ion channels (ASICs), showing equal or greater efficacy compared with
118 afferents possess acid sensing ion channels (ASICs), their contribution to the exercise pressor refle
119 osis can activate acid sensing ion channels (ASICs), we also studied ASIC1a(-/-) mice and found reduc
120 n and close human acid-sensing ion channels (ASICs), which are also trimers but are unrelated in sequ
121 The activation of acid-sensing ion channels (ASICs), which are highly permeable to calcium, has been
124 (Pyk2, ErbB1/2), pH-sensitive ion channels (ASICs, TASK, ROMK), and the bicarbonate-stimulated adeny
125 t other neurotransmitter-gated ion channels, ASICs show no desensitization during high-frequency stim
129 arent specific isentropic compressibilities, ASIC, were calculated from measured density, rho and spe
132 ercentage of muscle afferents that displayed ASIC-like currents, the current amplitudes, and the pH d
133 f the physiologic consequences of disrupting ASIC genes in mice suggested that ASIC channels might mo
134 4-AP has differential actions on distinct ASICs, strongly inhibiting ASIC1a channels expressed in
135 ammonium sensitivity is a widely distributed ASIC characteristic in the CNS, including the hippocampu
136 sitive pathway requires a conserved DEG/ENaC/ASIC mechanoreceptor complex in the FLP neuron pair.
142 ence of these currents in knock-out mice for ASIC-1a subunit (ASIC1a(-/-)) suggest that homomeric ASI
143 n the structure and on the pharmacophore for ASIC channel inhibition by mambalgins that could have th
144 by amiloride (100 microM, an antagonist for ASICs), tetrodotoxin (0.5 microM, a sodium channel block
147 Naked mole-rats, despite having functional ASICs, are insensitive to acid as a noxious stimulus and
150 subunit (ASIC1a(-/-)) suggest that homomeric ASIC-1as are mediating these currents in MNTB neurons.
151 ignificant characteristic of these homomeric ASIC-1as is their permeability to Ca(2+) Activation of A
152 ocked to model structures of homomeric human ASIC-1 to generate potential interaction sites and predi
161 Ca(2+) plays an important modulatory role in ASIC gating, competing with the ligand (H(+)) for its bi
163 10-fold sodium/potassium selectivity in ASICs has long been attributed to a central constriction
165 nder ischaemic conditions, and (3) increased ASIC(3) expression is largely observed in thin C-fibres
166 in A, an inhibitor of calcineurin, increased ASIC currents in Chinese hamster ovary cells and in cort
167 in slices, a pH drop from 7.4 to 7.0 induced ASIC-like inward currents (blocked by 100 muM amiloride)
168 hodopsin-3 (Arch), proton transients induced ASIC currents in both neurons and HEK293T cells co-expre
170 ASIC3 antagonist APETx2 reversibly inhibits ASIC-like currents in naked mole-rat dorsal root ganglia
171 ctivated proton pump recruited a slow inward ASIC current, which required molecular proximity of the
172 in extracellular pH induces transient inward ASIC currents (IASICs) in postsynaptic MNTB neurons from
173 ave revealed that postsynaptically localized ASICs contribute to the excitatory postsynaptic current
174 We conclude that ASIC2a and -3 are the major ASIC subunits in cardiac dorsal root ganglia neurons and
176 , endomorphin-1 (E-1) and -2 (E-2), modulate ASIC currents and the lactic acid-mediated pressor refle
177 a novel role for endomorphins in modulating ASIC function to effect lactic acid-mediated reflex incr
178 The results of anion substitution on native ASIC channels in hippocampal neurons mirrored those in h
179 1a homomers, ASIC1a/2a heteromers and native ASICs from sensory neurons to 1 ms acidification stimuli
180 idic transients, both recombinant and native ASICs show extremely rapid deactivation in outside-out p
181 and ASIC1a/2a heteromers, as well as native ASICs of sensory neurons, to follow trains of such brief
184 rize acid-induced current with activation of ASIC(3) in dorsal root ganglion (DRG) neurons of control
185 s their permeability to Ca(2+) Activation of ASIC-1a in MNTB neurons by exogenous H(+) induces an inc
188 study suggest that heteromeric complexes of ASIC and ENaC subunits may underlie the diversity of ami
189 has a profound effect on the contribution of ASIC and TRPV1 channels, therefore, altering the neurona
194 emistry was employed to examine existence of ASIC(3) expression in DRG neurons of thin-fibre afferent
199 he other hand, the biophysical properties of ASIC-like currents were significantly different in a sub
201 medulla including the VLM, and activation of ASICs in the VLM contributes to central chemoreception.
202 studies define mechanisms for activation of ASICs, illuminate the basis for dynamic ion selectivity
204 e demonstrate that the overall activities of ASICs, including channel activation, inactivation, and r
205 ortical neurons, suggesting that activity of ASICs is inhibited by calcineurin-dependent dephosphoryl
206 e, a licensed and clinically safe blocker of ASICs, was equally neuroprotective in nerve explants and
212 nduced a shift in the subunit composition of ASICs within muscle afferents, which significantly alter
214 at diminazene accelerates desensitization of ASICs, which was, however, not explained mechanistically
220 The molecular basis of NSAID inhibition of ASICs has remained unknown, hindering the exploration of
221 e aceturate is a small-molecule inhibitor of ASICs with a reported apparent affinity in the low micro
222 of the ASIC1a subunit, in the modulation of ASICs by oxidizing and reducing agents, respectively.
224 The wide and varied expression patterns of ASICs, BK, and related K(+) channels suggest broad oppor
226 results will help us understand the role of ASICs in exercise physiology and provide a molecular tar
227 ay help in understanding the precise role of ASICs in physiological and pathological conditions at di
229 ests that activation of ASIC1a, a subtype of ASICs that is widely distributed in the brain, is necess
230 efly review advances in our understanding of ASICs, their potential contributions to disease, and the
231 d accumulation in exercising muscle acted on ASICs located on thin fibre muscle afferents to evoke th
236 d inactivation curves of ASIC3 but not other ASICs overlap in the presence of GMQ at pH 7.4, thereby
239 ontributions of ASIC1a and ASIC2a to overall ASIC-mediated responses undergo distinct developmental c
240 Furthermore, the activation of postsynaptic ASIC-1as during high-frequency stimulation (HFS) of the
241 tter-gated ion channels because postsynaptic ASICs can be activated by the transient acidification of
242 ver, evidence for activation of postsynaptic ASICs during neurotransmission has not been established.
243 ypothesis is that activation of postsynaptic ASICs promotes depolarization, thereby augmenting N-meth
244 n acidic solutions significantly potentiated ASIC currents when compared to acidic solutions alone.
245 nhibit with the same pharmacological profile ASIC channels to exert strong analgesic effects in vivo.
246 likely to occur at the cleft and may provide ASICs with the ability to shape activity in response to
249 A binding to AKAPs by Ht-31 peptide reduces ASIC currents in cortical neurons and Chinese hamster ov
252 d that the ascidian genome contains a single ASIC gene that gives rise to two splice forms analogous
264 Therefore, we tested the hypothesis that ASIC channels might inhibit K(+) channel function by coe
265 ings are consistent with the hypothesis that ASIC-3 plays a protective role in the inflammatory arthr
266 microscopy and co-immunoprecipitation, that ASIC and ENaC subunits are capable of forming cross-clad
268 hese observations raise the possibility that ASIC channels function as coincidence detectors for extr
269 l analysis of dye-filled neurons showed that ASIC-dependent chemosensitive cells (cells responding to
270 disrupting ASIC genes in mice suggested that ASIC channels might modulate neuronal function by mechan
273 The results provide the first evidence that ASICs may contribute to chemotransduction of low pH by c
274 nd further mutagenesis provide evidence that ASICs show such steeply agonist-dependent deactivation b
279 minazene and its binding site on ASIC1a, the ASIC subunit with the greatest importance in the central
283 ts, however it is not yet clear which of the ASIC subunits contribute to the composition of ASICs in
286 is known that a drop in pH(o) activates the ASICs, it is not clear whether alterations of pH(i) have
290 ng and inactivating current mediated through ASICs, and a slow sustaining current via activation of T
292 ent proton-transporting optogenetic tools to ASICs to create two-component optogenetic constructs (TC
294 Furthermore, pH reduction triggered typical ASIC-type currents in the medulla, including the VLM.
296 he purpose of this study was to test whether ASIC-3-deficient mice with arthritis have altered inflam
298 Moreover, the percentage of DRG neurons with ASIC(3)-like currents is greater after arterial occlusio
299 receptors that form a molecular complex with ASICs; the receptor on sensory neurons appears to be P2X
WebLSDに未収録の専門用語(用法)は "新規対訳" から投稿できます。