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1 n (c.4447G>A; p.E1483K) in SCN8A, encoding a voltage-gated sodium channel.
2 ic causes are mutations in Nav1.1 (SCN1A), a voltage-gated sodium channel.
3 rom wild-type and epilepsy-associated mutant voltage-gated sodium channels.
4 latus that delays inactivation of vertebrate voltage-gated sodium channels.
5  between activation and fast inactivation in voltage-gated sodium channels.
6 ing p38 MAPK-mediated negative modulation of voltage-gated sodium channels.
7  and fails to recruit neurofascin as well as voltage-gated sodium channels.
8  in the immature brain through alteration of voltage-gated sodium channels.
9 clusters for gliomedin, neurofascin-186, and voltage-gated sodium channels.
10 ibution from entry through NMDA receptors or voltage-gated sodium channels.
11 om tarantula venom able to inhibit the human voltage-gated sodium channel 1.7 (hNaV1.7), a channel re
12                        The prominent role of voltage-gated sodium channel 1.7 (Nav1.7) in nociception
13                                          The voltage-gated sodium channel 1.7 (Nav1.7) plays an impor
14 ipheral expression of tetrodotoxin-resistant voltage-gated sodium channel 1.8 (NaV1.8) has been shown
15 , in mice, this effect is mediated solely by voltage-gated sodium channel 1.8 (NaV1.8).
16                  The location of the gate in voltage-gated sodium channels, a founding member of this
17 Cone snail toxins are well known blockers of voltage-gated sodium channels, a property that is of bro
18 g shift of tetrodotoxin-sensitive persistent voltage-gated sodium channel activation.
19 annels, Kir2.1 and dORKDelta-C) or decreased voltage-gated sodium channel activity (using mutations i
20 NRG1 are primarily attributable to decreased voltage-gated sodium channel activity, as current densit
21 maging in rat slices, we find that dendritic voltage-gated sodium channels allow somatic action poten
22        The mutations in the coding region of voltage-gated sodium channel alpha 1 subunit gene, SCN1A
23              However, expression analysis of voltage-gated sodium channel alpha subunits revealed NaV
24 a2-subunits in the ventricle is to chaperone voltage-gated sodium channel alpha-subunits to the plasm
25 ts proposed biological targets include human voltage-gated sodium channels, among other membrane prot
26 inactivated conformational cycle in a single voltage-gated sodium channel and give insight into the s
27 sity accommodate the atomic coordinates of a voltage-gated sodium channel and of the beta subunit in
28 lication of thrombin did not alter transient voltage-gated sodium channels and action potential thres
29 te loss of nodal protein staining, including voltage-gated sodium channels and ankyrin G, occurs and
30 enous cannabinoids have been shown to target voltage-gated sodium channels and cannabidiol has recent
31 but allosterically coupled receptor sites on voltage-gated sodium channels and cause persistent chann
32 n II and to the pore module of domain III in voltage-gated sodium channels and enhance channel activa
33 s required for the interaction of FGF14 with voltage-gated sodium channels and neuronal excitability.
34 rs and not through NMDA receptors or through voltage-gated sodium channels and that the spine neck is
35 led the peptide's putative molecular target (voltage-gated sodium channels) and mechanism of action (
36 f the interactions between CBD and the NavMs voltage-gated sodium channel, and electrophysiology to s
37 eurofascin, neuronal cell adhesion molecule, voltage-gated sodium channels, and actin filaments.
38 ts, at least in part, through its actions on voltage-gated sodium channels, and resurgent current may
39 urons, which express a unique combination of voltage-gated sodium channels; and (3) heterologously ex
40                                              Voltage gated sodium channels are key players in aberran
41                                    Mammalian voltage-gated sodium channels are composed of four homol
42                                              Voltage-gated sodium channels are critical determinants
43                                    ABSTRACT: Voltage-gated sodium channels are critical for neuronal
44                                              Voltage-gated sodium channels are critical for periphera
45               Activation and inactivation of voltage-gated sodium channels are critical for proper el
46                                              Voltage-gated sodium channels are crucial determinants o
47                  Fast opening and closing of voltage-gated sodium channels are crucial for proper pro
48                                              Voltage-gated sodium channels are essential for electric
49                                              Voltage-gated sodium channels are important targets for
50                                              Voltage-gated sodium channels are inhibited by many loca
51 ate, we provide novel evidence that multiple voltage-gated sodium channels are involved in schizophre
52       In this study, we investigated whether voltage-gated sodium channels are involved in the develo
53                                              Voltage-gated sodium channels are required for the initi
54                                              Voltage-gated sodium channels are responsible for action
55                                              Voltage-gated sodium channels are subjected to S-palmito
56                                              Voltage-gated sodium channels are targets for a range of
57                                However, when voltage-gated sodium channels are temporarily blocked, c
58                                              Voltage-gated sodium channels are the primary target of
59                       The mechanism by which voltage-gated sodium channels are trafficked to the surf
60                                              Voltage-gated sodium channels are vital membrane protein
61          Variants in SCN10A, which encodes a voltage-gated sodium channel, are associated with altera
62  muscle channel (SCN4A), encoding the Nav1.4 voltage-gated sodium channel, are causative of a variety
63         These results show that BBG inhibits voltage-gated sodium channels at micromolar concentratio
64 l isoform of Neurofascin, Nfasc186, clusters voltage-gated sodium channels at nodes of Ranvier in mye
65 myelinated nerves requires the clustering of voltage-gated sodium channels at nodes of Ranvier.
66 myelinating Schwann cells, such as clustered voltage-gated sodium channels at the node of Ranvier and
67  deficient for exon 1b, PV interneurons lack voltage-gated sodium channels at their axonal initial se
68 e secretases also regulate the processing of voltage-gated sodium channel auxiliary beta-subunits and
69 GIC behavior, we addressed how the bacterial voltage-gated sodium channel (BacNa(V)) C-terminal cytop
70 es of members of a large family of bacterial voltage-gated sodium channels (BacNa(V)s) prevalent in s
71                                    Bacterial voltage-gated sodium channels (BacNavs) serve as models
72 omologous factors (FHFs) bound to axosomatic voltage-gated sodium channels bear an N-terminal blockin
73                    Identified genes included voltage-gated sodium channel beta subunits, potassium ch
74                 Mutations in SCN2B, encoding voltage-gated sodium channel beta2-subunits, are associa
75 nts revealed that Ae1a potently inhibits the voltage-gated sodium channel BgNaV1 from the German cock
76 teractions between scaffolding molecules and voltage-gated sodium channels, but the molecular mechani
77 tion, pyridine nucleotides also modulate the voltage-gated sodium channel by supporting the activity
78 f cone snails, known as mu-conotoxins, block voltage-gated sodium channels by physically occluding th
79                        Key among them is the voltage-gated sodium channel complex.
80                                              Voltage-gated sodium channels comprise an ion-selective
81  also found alterations in the properties of voltage-gated sodium channel currents in Jedi-1 null neu
82 des (P<0.0001), with altered architecture of voltage-gated sodium channel distribution.
83  in a reduction in the fraction of available voltage-gated sodium channels due to insufficient recove
84 polychlorocyclohexanes and fiproles, and the voltage-gated sodium channel for pyrethroids and dichlor
85  complexes often considered independent: the voltage-gated sodium channel, gap junctions, and the car
86 T. urticae populations and a mutation in the voltage-gated sodium channel gene (F1538I) in 66.7% popu
87 n Culex quinquefasciatus display CNV for the voltage-gated sodium channel gene (Vgsc), target-site of
88               Missense variants in the SCN8A voltage-gated sodium channel gene are linked to early-in
89 gous loss-of-function mutations in the brain voltage-gated sodium channel gene SCN1A.
90                     De novo mutations of the voltage-gated sodium channel gene SCN8A have recently be
91  caused by de novo missense mutations in the voltage-gated sodium channel gene SCN8A Here, we investi
92 eased in number in larvae that have a mutant voltage-gated sodium channel gene, scn8aa.
93 e mutation (c.5302A>G [p.Asn1768Asp]) in the voltage-gated sodium-channel gene SCN8A in the proband.
94 erity have been associated with mutations in voltage-gated sodium channel genes.
95    Although a gate residue in the eukaryotic voltage-gated sodium channel has been identified, the mi
96                         Slow inactivation of voltage-gated sodium channels has been discussed to be t
97                              The activity of voltage-gated sodium channels has long been linked to di
98               Mutations in brain isoforms of voltage-gated sodium channels have been identified in pa
99                                              Voltage-gated sodium channels have essential roles in el
100                                    The human voltage-gated sodium channel, hNa(V)1.5, is responsible
101 alanine 1486 (F1486del) in the human cardiac voltage-gated sodium channel (hNav1.5) is associated wit
102 A SIGNIFICANCE STATEMENT Na(v)1.6 is a major voltage-gated sodium channel in human brain, where it re
103 f variants in SCN5A, which encodes the major voltage-gated sodium channel in the heart.
104                  Na(v)1.6 (SCN8A) is a major voltage-gated sodium channel in the mammalian CNS, and i
105 trocytes in vitro have been shown to express voltage-gated sodium channels in a dynamic manner, with
106         Human studies have firmly implicated voltage-gated sodium channels in human pain disorders, a
107                           Na(v)1.7 and other voltage-gated sodium channels in mouse DRG are considere
108  now linked multiple human pain disorders to voltage-gated sodium channels, including disorders chara
109 hree disulfide bridges, is a pore blocker of voltage-gated sodium channels, including neuronal subtyp
110                                              Voltage-gated sodium channels initiate action potentials
111                                              Voltage-gated sodium channels initiate action potentials
112                                              Voltage-gated sodium channels initiate electrical signal
113                                   The Nav1.1 voltage-gated sodium channel is a critical contributor t
114   The ion translocation process seen in this voltage-gated sodium channel is clearly different from t
115                                          The voltage-gated sodium channel is critical for cardiomyocy
116                                   The NaV1.7 voltage-gated sodium channel is implicated in human pain
117 congenital insensitivity to pain (CIP); this voltage-gated sodium channel is therefore a key target f
118                       Ion permeation through voltage-gated sodium channels is modulated by various dr
119                                Inhibition of voltage-gated sodium channels is neuroprotective in prec
120 gia, the first human pain syndrome linked to voltage-gated sodium channels, is widely regarded as a g
121                        Nav1.6 is the primary voltage-gated sodium channel isoform expressed in mature
122                                          The voltage-gated sodium channel isoform Na(V)1.7 is highly
123 at, while VPA is capable of binding to these voltage-gated sodium channels, it has a very different m
124 1-type sodium channels and to substitute for voltage-gated sodium channels lacking in many invertebra
125 utations in Nav.1.7, the main pain signaling voltage-gated sodium channel, lead to its truncations an
126 ive axonal potentials that are maintained by voltage-gated sodium channels, leading to a declination
127 hether manipulation of splicing of mammalian voltage-gated sodium channels may be exploitable to prov
128 e results suggest that altered processing of voltage-gated sodium channels may contribute to aberrant
129 ular determinants of toxin interactions with voltage-gated sodium channels may permit development of
130                                       Axonal voltage-gated sodium channel mRNA and local trafficking
131                               The finding of voltage-gated sodium channel mutations in small fibre ne
132                              The sarcolemmal voltage gated sodium channel Na(V)1.4 conducts the key d
133 ant mutations in the SCN1A gene encoding the voltage-gated sodium channel Na(v) 1.1.
134 aploinsufficiency of the SCN1A gene encoding voltage-gated sodium channel Na(V)1.1 causes Dravet's sy
135             Mutations in SCN1A, encoding the voltage-gated sodium channel Na(V)1.1, are the most comm
136 sufficiency of the SCN1A gene encoding brain voltage-gated sodium channel Na(V)1.1.
137   Mutations in the gene encoding the cardiac voltage-gated sodium channel Na(v)1.5 cause various card
138                                              Voltage-gated sodium channel Na(v)1.5 generates cardiac
139                    The function of the human voltage-gated sodium channel Na(V)1.5 is regulated in pa
140 tage-gated potassium channel K(V)1.3 and the voltage-gated sodium channel Na(V)1.7 as examples of tar
141       Gain-of-function missense mutations of voltage-gated sodium channel Na(V)1.7 have been linked t
142                                              Voltage-gated sodium channel Na(V)1.7 is a genetically v
143                                          The voltage-gated sodium channel Na(V)1.7 is believed to be
144            In humans, functional loss of the voltage-gated sodium channel Na(v)1.7 leads to pain inse
145                                          The voltage-gated sodium channel Na(v)1.7 plays a crucial ro
146 ansient receptor potential channel TRPA1 and voltage-gated sodium channel Na(v)1.7, that accompany al
147 FN for mutations in the SCN9A gene, encoding voltage-gated sodium channel Na(V)1.7, which is preferen
148                            SCN9A encodes the voltage-gated sodium channel Na(v)1.7, which is present
149                                          The voltage-gated sodium channel Na(v)1.8 is known to functi
150 monstrates that two disease mutations in the voltage-gated sodium channel Na(v)1.8 that induce nocice
151 ination of a high-resolution 3D structure of voltage-gated sodium channel Na(V)Ab opens the way to el
152 ins, PIIIA, effectively blocks the bacterial voltage-gated sodium channel Na(V)Ab, whose crystal stru
153                                              Voltage-gated sodium channels Na(v)1.2 and Na(v)1.6 are
154 ch information learned in recent years about voltage gated sodium channel (Na(V)) subtypes in somatos
155              A biophysical analysis revealed voltage-gated sodium channel (Na(V)) currents in menthol
156                                  The cardiac voltage-gated sodium channel (Na(V)1.5) underlies impuls
157                            Human nociceptive voltage-gated sodium channel (Na(v)1.7), a target of sig
158 n dissection, that the Silicibacter pomeroyi voltage-gated sodium channel (Na(V)Sp1) PD forms a stand
159  Peripheral sensory neurons express multiple voltage-gated sodium channels (Na(V) ) critical for the
160 trodotoxin (TTX), a neurotoxin that binds to voltage-gated sodium channels (Na(v) proteins), arrestin
161                                              Voltage-gated sodium channels (Na(V)) are indispensable
162                                              Voltage-gated sodium channels (Na(v)) underlie the rapid
163  alpha-toxins affect insect and/or mammalian voltage-gated sodium channels (Na(v)s) and thereby modif
164      The tremendous therapeutic potential of voltage-gated sodium channels (Na(v)s) has been the subj
165                                              Voltage-gated sodium channels (Na(v)s) initiate the acti
166                                              Voltage-gated sodium channels (Na(V)s) provide the initi
167                                              Voltage-gated sodium channels (Na(V)s) underlie the upst
168  nefarious effects result from inhibition of voltage-gated sodium channels (Na(V)s), the obligatory p
169 uit of novel subtype-selective modulators of voltage-gated sodium channels (Na(v)s).
170 s of sodium conductance across membranes are voltage-gated sodium channels (Na(V)s).
171 r the ion transport function mediated by the voltage-gated sodium channel, Na(V)1.2.
172 nce-conferring amino acid substitutions in a voltage-gated sodium channel, Na(v)1.4, are clustered in
173                                        Three voltage-gated sodium channels, Na(v)1.7, Na(v)1.8, and N
174 quantify isoflurane binding to the bacterial voltage-gated sodium channel NaChBac.
175                                    ABSTRACT: Voltage-gated sodium channel NaV 1.7 is required for acu
176 binds to the domain II voltage sensor in the voltage-gated sodium channel Nav and modifies its voltag
177                                              Voltage-gated sodium channel (NaV) mutations cause genet
178                                              Voltage-gated sodium channel (NaV) trafficking is incomp
179  metabotropic glutamate receptor-1 (mGluR1), voltage-gated sodium channels (Nav ) and glutamate trans
180 Ts3 binds to the domain IV voltage sensor of voltage-gated sodium channels (Nav ) and slows down thei
181 phibian prey, which select for TTX-resistant voltage-gated sodium channels (Nav) [12-16].
182                             They are rich in voltage-gated sodium channels (Nav) and thus underpin ra
183 myelinated nerves requires the clustering of voltage-gated sodium channels (Nav) at nodes of Ranvier
184 heless, Nfasc140, like Nfasc186, can cluster voltage-gated sodium channels (Nav) at the developing no
185                We examined the repertoire of voltage-gated sodium channels (NaV) in fluorescence-sort
186 mans and other vertebrates, target conserved voltage-gated sodium channels (NaV) of nerve and muscle,
187                                              Voltage-gated sodium channels (NaV) play an important ro
188  and whether human SAN excitability requires voltage-gated sodium channels (Nav) remains controversia
189 ic tension, the thermal random motion of the voltage-gated sodium channels (Nav), which are bound to
190 Conotoxins act by inhibiting inactivation of voltage-gated sodium channels (Nav).
191                         The beta1 subunit of voltage-gated sodium channels, Nav beta1, plays multiple
192 n the SCN1A gene, which encodes brain type-I voltage-gated sodium channel NaV1.1.
193 d by loss-of-function mutations in the brain voltage-gated sodium channel NaV1.1.
194 of an adjacent gene (SCN2A) coding for human voltage-gated sodium channel NaV1.2 (P = 9 x 10(-4)).
195      Mutations in SCN2A, a gene encoding the voltage-gated sodium channel Nav1.2, have been associate
196        Therefore, EC cells use Scn3a-encoded voltage-gated sodium channel NaV1.3 for electrical excit
197 ed a critical role for the regulation of the voltage-gated sodium channel NaV1.5 in the heart by the
198   We investigated the effect of LITAF on the voltage-gated sodium channel Nav1.5, which is critical f
199       SCN5A encodes the alpha-subunit of the voltage-gated sodium channel NaV1.5.
200                           This is due to the voltage-gated sodium channel Nav1.7 (Scn9a), previously
201 ates that the expression and function of the voltage-gated sodium channel Nav1.7 are increased in a p
202                             Mutations in the voltage-gated sodium channel Nav1.7 are linked to inheri
203    Human genetic studies have implicated the voltage-gated sodium channel NaV1.7 as a therapeutic tar
204 inflammatory pain requires the expression of voltage-gated sodium channel Nav1.7 but its significance
205 unction mutations in the SCN9A gene encoding voltage-gated sodium channel Nav1.7 cause congenital ins
206                                              Voltage-gated sodium channel Nav1.7 is a central player
207                           Trafficking of the voltage-gated sodium channel NaV1.7 is dysregulated in n
208                                    The human voltage-gated sodium channel Nav1.7 plays a crucial role
209                Gain-of-function mutations of voltage-gated sodium channel Nav1.7 underlie dorsal root
210                       Functional variants of voltage-gated sodium channel Nav1.7, encoded by SCN9A, h
211 iant in the second intracellular loop of the voltage-gated sodium channel NaV1.7, encoded by the SCN9
212 ndromes have been linked to mutations in the voltage-gated sodium channel Nav1.7.
213          Under physiological conditions, the voltage-gated sodium channel Nav1.8 is expressed almost
214 notoxins MrVIA, MrVIB, and MfVIA inhibit the voltage-gated sodium channel NaV1.8, a well described ta
215 ies have confirmed an important role for the voltage-gated sodium channel Nav1.9 in human pain disord
216 dromes, and variants of genes coding for the voltage-gated sodium channels Nav1.8 (SCN10A) and Nav1.9
217 nsfer (LRET) between the rat skeletal muscle voltage-gated sodium channel (Nav1.4) and fluorescently
218 des the alpha-subunit of the skeletal muscle voltage-gated sodium channel (Nav1.4).
219            Gain-of-function mutations in the voltage-gated sodium channel (Nav1.5) are associated wit
220                                      Cardiac voltage-gated sodium channels (Nav1.5) play an essential
221 ge-gated sodium channel (SCN5A gene encoding voltage-gated sodium channel [NaV1.5]) cause congenital
222 c evidence has clearly demonstrated that the voltage-gated sodium channel, Nav1.7, is critical to pai
223 multiple elements within the promoter of the voltage-gated sodium channel, Nav1.7, leading to a syner
224         The X-ray structure of the bacterial voltage-gated sodium channel NavAb has been reported in
225 enic mice, also cleaves the beta2-subunit of voltage-gated sodium channels (Navbeta2).
226                                              Voltage-gated sodium channels (NaVs) are activated by tr
227                                              Voltage-gated sodium channels (NaVs) are central element
228                                 Mutations in voltage-gated sodium channels (Navs) can cause alteratio
229  It is characterized by the dysregulation of voltage-gated sodium channels (Navs) expressed in dorsal
230                                              Voltage-gated sodium channels (Navs) play crucial roles
231                                              Voltage-gated sodium channels (Navs) play essential role
232                         Improper function of voltage-gated sodium channels (NaVs), obligatory membran
233  in part due to changes in the properties of voltage-gated sodium channels (Navs).
234 ty resulting from point mutations within the voltage-gated sodium channel of the insect nervous syste
235  These results suggest that sanshool targets voltage-gated sodium channels on Adelta mechanosensory n
236 ptic drug carbamazepine was found to inhibit voltage-gated sodium channels only with external, but no
237  at paralog-conserved sites were enriched in voltage-gated sodium channels, particularly the alpha su
238                                              Voltage-gated sodium channels play a critical role in ce
239                                  KEY POINTS: Voltage-gated sodium channels play a fundamental role in
240                                      Whereas voltage-gated sodium channels play a well known and impo
241 ture of the open conformation of a bacterial voltage-gated sodium channel pore from Magnetococcus sp.
242 ut not blockers of AMPA/kainate receptors or voltage-gated sodium channels, prevented microglial outg
243 oltage dependence of the rat skeletal muscle voltage-gated sodium channel rNav1.4 expressed in oocyte
244                    Mutations in the neuronal voltage-gated sodium channel SCN1A are associated with a
245 revealed that the didy mutation disrupts the voltage-gated sodium channel Scn1lab (Nav1.lb).
246                     Mutations of the cardiac voltage-gated sodium channel (SCN5A gene encoding voltag
247 tiated and propagated by a single isoform of voltage gated sodium channels - SCN5A.
248 euritis at concentrations at which it blocks voltage-gated sodium channels selectively.
249  of organic cation selectivity of eukaryotic voltage-gated sodium channels showed a sharp size cut-of
250 perties were independent of modifications in voltage-gated sodium channels since 100 nM bifenthrin ha
251 ilayer affinity and in vitro activity at the voltage-gated sodium channel subtype 1.7 (Na(V)1.7), a c
252                                Specifically, voltage-gated sodium channel subtype NaV 1.7 is required
253 tations in the human SCN1A gene encoding the voltage-gated sodium channel subunit Nav 1.1.
254 interneuron-specific and PV cell-predominant voltage-gated sodium channel subunit Nav1.1.
255 xpression of a human-specific isoform of the voltage-gated sodium channel subunit SCN4B was significa
256 CN10A, which encodes a nociceptor-associated voltage-gated sodium channel subunit, as a modulator of
257 ciated with the cleavage of Neuregulin and a voltage-gated sodium channel subunit.
258  the central nervous system (CNS) containing voltage-gated sodium channels targeted by deltamethrin.
259    Thus, structural properties of eukaryotic voltage-gated sodium channels that are suggested by func
260 ed and likely to have evolved from ancestral voltage-gated sodium channels that are widely expressed
261  that heterologously expressed human cardiac voltage-gated sodium channel, the principle cardiac sodi
262  knockdown, alter splicing of the Drosophila voltage-gated sodium channel to favour inclusion of exon
263 um2 is able to directly bind the predominant voltage-gated sodium channel transcript (NaV1.6) express
264             We determined the structure of a voltage-gated sodium channel, two-pore channel 3 (TPC3),
265                                              Voltage-gated sodium channels underlie the rapid regener
266 mutation in SCN11A, which encodes the Nav1.9 voltage-gated sodium channel, underlies a human disorder
267 osequencing genotyping and sequencing of the voltage gated sodium channel (VGSC) gene did not detect
268                                              Voltage-gated sodium channel (VGSC) activity has previou
269                                              Voltage-gated sodium channel (VGSC) beta subunits signal
270                                              Voltage-gated sodium channel (VGSC) beta1 subunits are m
271 plasticity, we used brevetoxin-2 (PbTx-2), a voltage-gated sodium channel (VGSC) gating modifier, to
272                       Veratridine (VTD) is a voltage-gated sodium channel (VGSC) modifier that is use
273                                              Voltage-gated sodium channel (VGSC) mutations cause seve
274 ecent genetic studies have linked pathogenic voltage-gated sodium channel (VGSC) variants to human pa
275  mutations L1014F and L1014S within the para voltage-gated sodium channel (VGSC).
276 -14) bind to the C termini (CTs) of specific voltage-gated sodium channels (VGSC) and thereby regulat
277                                              Voltage-gated sodium channels (VGSC) are transmembrane p
278                      We hypothesize that the voltage-gated sodium channels (VGSC) on the dorsal root
279                                     Notably, voltage-gated sodium channels (VGSC) that are crucial fo
280 agnitude shorter than the activation time of voltage-gated sodium channels (VGSC) would evoke action
281 s to efficiently overexpress large mammalian voltage-gated sodium channels (VGSC).
282 f structural and functional relationships of voltage-gated sodium channels (VGSC).
283 sed to contribute to anesthetic effects, the voltage gated sodium channels (VGSCs) should also be con
284 ies of myelinated fibres, however, show that voltage-gated sodium channels (VGSCs) aggregate with cel
285             KCNQ2/3 (Kv7.2/7.3) channels and voltage-gated sodium channels (VGSCs) are enriched in th
286                                              Voltage-gated sodium channels (VGSCs) are essential to t
287                                              Voltage-gated sodium channels (VGSCs) are important for
288                                              Voltage-gated sodium channels (VGSCs) are responsible fo
289 benzyl-3-methoxypropanamide (LCM)) modulates voltage-gated sodium channels (VGSCs) by preferentially
290           We have recently demonstrated that voltage-gated sodium channels (VGSCs) in dorsal root gan
291  nodes of Ranvier are sites of clustering of voltage-gated sodium channels (VGSCs) in nervous systems
292                                              Voltage-gated sodium channels (VGSCs) regulate invasion
293                                Clustering of voltage-gated sodium channels (VGSCs) within the neurona
294 thrombin effect on neuronal excitability and voltage-gated sodium channels was assessed using extrace
295             Kidins220 association with brain voltage-gated sodium channels was shown by co-immunoprec
296  acts on various targets in vitro, including voltage-gated sodium channels, was initially proposed as
297 cing the primary pyrethroid target site, the voltage-gated sodium channel, we show that point mutatio
298 rt toxic effects by altering the function of voltage-gated sodium channels, which are essential for p
299  in mammals, nine genes encode nine distinct voltage-gated sodium channels with different amino acid
300                                  Blockade of voltage-gated sodium channels with TTX and reverse (Ca(2

 
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