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1 uter vestibule and selectivity region of the voltage-gated Na channel.
2 titive antagonists of batrachotoxin (BTX) in voltage-gated Na+ channels.
3 ), have played crucial roles in the study of voltage-gated Na+ channels.
4  its clinically important action by blocking voltage-gated Na+ channels.
5 ackbone location of S5 and S6 helices of the voltage-gated Na(+) channel.
6 N4A gene, encoding the human skeletal muscle voltage-gated Na(+) channel.
7 nels in a manner that resembles the block of voltage-gated Na(+) channels.
8  removal of Ca(2+), but not by a blockade of voltage-gated Na(+) channels.
9 gnificant homology with the beta2 subunit of voltage-gated Na(+) channels.
10  inhibit Na(+) flux by occluding the pore of voltage-gated Na(+) channels.
11 e best known for their inhibitory effects on voltage-gated Na(+) channels.
12 val and partially protected by a blockade of voltage-gated Na(+) channels.
13 of repriming (recovery from inactivation) of voltage-gated Na(+) channels.
14  similarity between bacterial and eukaryotic voltage-gated Na(+) channels.
15 otential and graded potential models lacking voltage-gated Na(+) channels.
16 mbrane excitability, and the localization of voltage-gated Na(+) channels.
17 ion channels in the heart, including cardiac voltage-gated Na(+) channels.
18 lar to voltage-gated Ca(2+) channels than to voltage-gated Na(+) channels.
19       The AII processes showed clustering of voltage-gated Na+ channel 1.1 (Na(v)1.1) as well as AIS
20 ting that ipRGC-to-DAC transmission requires voltage-gated Na(+) channels; (2) this transmission is p
21 ion of pyrethroids with the alpha subunit of voltage-gated Na+ channels, a radioactive photosensitive
22 hannel complexes unexpectedly identified the voltage-gated Na(+) channel accessory subunit Navbeta1.
23 ound, we modified only the properties of the voltage-gated Na(+) channel according to our patch-clamp
24 gulate TEP and JI Epistasis assays show that voltage-gated Na(+) channels act downstream of H2O2 to m
25                                More broadly, voltage-gated Na channels adopt this same modulatory pri
26                 Mutations in segment IVS6 of voltage-gated Na(+) channels affect fast-inactivation, s
27 ecombinant brain, skeletal muscle, and heart voltage-gated Na+ channel alpha subunits differ in their
28                                          The voltage-gated Na+ channel alpha-subunit consists of four
29             Two mutant human skeletal muscle voltage-gated Na+ channel alpha-subunits (hSkM1), with m
30                        Na(V)1.5 is a cardiac voltage-gated Na(+) channel alphasubunit and is encoded
31 esterone had little or no effect on a cloned voltage-gated Na+ channel, an inward rectifier K+ channe
32      Our report demonstrates that a specific voltage-gated Na(+) channel and its associated impairmen
33     Batrachotoxin (BTX) alters the gating of voltage-gated Na(+) channels and causes these channels t
34 270-kD and participates in the clustering of voltage-gated Na(+) channels and cell-adhesion molecules
35                                  BTX targets voltage-gated Na(+) channels and enables them to open pe
36                 Mechanistically, 4 inhibited voltage-gated Na(+) channels and N-type Ca(2+) channels
37                Mechanistically, 4a inhibited voltage-gated Na(+) channels and N-type Ca(2+) channels
38 rns the identification of different types of voltage-gated Na(+) channels and of muscarinic and purin
39        We examined the kinetic properties of voltage-gated Na(+) channels and their contribution to t
40         VTD causes persistent opening of the voltage-gated Na+ channel and reduces its single-channel
41 day 7 (P7), almost all node-like clusters of voltage-gated Na+ channels and ankyrinG are adjacent to
42 suggest the following: node-like clusters of voltage-gated Na+ channels and ankyrinG form adjacent to
43 nitric oxide production), Na+ influx through voltage-gated Na+ channels and axonal AMPA receptors, re
44 ernal QX and local anaesthetic pore block of voltage-gated Na+ channels and provide insight into unde
45 arbamazepine, and lamotrigine block neuronal voltage-gated Na(+) channels, and their binding sites to
46 epends strongly, although not completely, on voltage-gated Na+ channels, and the spatial extent of fe
47                                              Voltage-gated Na(+) channels are composed of pore-formin
48                                              Voltage-gated Na(+) channels are critical components in
49                                              Voltage-gated Na(+) channels are critical determinants o
50                                              Voltage-gated Na(+) channels are the primary targets of
51                                              Voltage-gated Na(+) channels are the workhorses of spike
52                                              Voltage-gated Na(+)-channels are transmembrane proteins
53                                              Voltage-gated Na+ channels are a primary target for loca
54                                              Voltage-gated Na+ channels are essential for the normal
55                                              Voltage-gated Na+ channels are major targets of G protei
56                                              Voltage-gated Na+ channels are the molecular targets of
57              This study examined the loss of voltage-gated Na+ channels as well as acetylcholine rece
58 (Nfasc186) is required for the clustering of voltage gated Na+ channels at the node, whilst the 155 k
59                    This evidence for loss of voltage-gated Na+ channels at the motor end plate in bot
60 rity was not caused solely by a reduction in voltage-gated Na(+) channel availability.
61 mechanism was not via Na+ influx through the voltage-gated Na+ channels because the release was not a
62                                              Voltage-gated Na(+) channel beta1 subunits are multifunc
63                             We conclude that voltage-gated Na(+) channel beta1 subunits signal via mu
64                                          The voltage-gated Na+ channel blocker tetrodotoxin (TTX) abo
65  that FHFs not only are potent modulators of voltage-gated Na+ channels but also affect Ca2+ channels
66 s; FGF11-14) are intracellular modulators of voltage-gated Na+ channels, but their cellular distribut
67                                   Opening of voltage-gated Na+ channels by application of 50 microM v
68          Expression of mRNA encoding several voltage-gated Na+ channels by the E11.5 gut was detected
69 s of the myelin-deficient rat, which contain voltage-gated Na(+) channel clusters but lack paranodal
70 rated function of a molecular aggregate (the voltage-gated Na(+) channel complex) that includes the b
71 (85%), suggesting that influx of Na+ through voltage-gated Na+ channels contributed to baseline [Na+]
72 with previous suggestions, the activation of voltage-gated Na(+) channels contributes to axonal damag
73 al communication; and (3) Na+ influx through voltage-gated Na+ channels could be important to fuel th
74 failure is associated with decreased cardiac voltage-gated Na+ channel current (encoded by SCN5A), an
75                                              Voltage-gated Na(+) channels display rapid activation ga
76 lly identified by its sequence similarity to voltage-gated Na(+) channels, encodes a functional volta
77 h less is known about developmental roles of voltage-gated Na+ channels, essential mediators of elect
78  a gene that encodes an auxiliary protein of voltage-gated Na(+) channels, fibroblast growth factor 1
79    Here we report the crystal structure of a voltage-gated Na(+) channel from Arcobacter butzleri (Na
80  Local anesthetic antiarrhythmic drugs block voltage-gated Na(+) channels from the cytoplasmic side.
81 nomic studies have revealed that animal-type voltage-gated Na(+) channels had evolved in choanoflagel
82 in (TTX, 1 microM), a selective inhibitor of voltage-gated Na(+) channels, had an effect on mechanica
83 hese oscillations required the activation of voltage-gated Na(+) channels, had the same frequency as
84      Here we introduce roNaV2, an engineered voltage-gated Na(+) channel harboring a selenocysteine i
85 sense mutations of the human skeletal muscle voltage-gated Na channel (hSkM1) underlie a variety of d
86  proliferated and coexpressed PDGFRalpha and voltage-gated Na(+) channels (I(Na)).
87                                The principal voltage-gated Na channel in heart, Nav1.5, is directly a
88      Ankyrin-G associates with the principal voltage-gated Na channel in the heart, and loss of this
89                                              Voltage-gated Na channels in many neurons, including sev
90                                              Voltage-gated Na channels in several classes of neurons,
91                      Na(V)1.1 is the primary voltage-gated Na(+) channel in several classes of GABAer
92                                              Voltage-gated Na(+) channels in the brain are composed o
93 temperature increases the ion influx through voltage-gated Na(+) channels in the cold sensory nerve e
94           Batrachotoxin (BTX) stabilizes the voltage-gated Na(+) channels in their open conformation,
95 the first time the molecular identity of the voltage-gated Na+ channel in freshly dispersed smooth mu
96                The function of BNC1 as a non-voltage-gated Na+ channel in human brain suggests it may
97                      Kv3.1b colocalizes with voltage-gated Na+ channels in a subset of nodes in the s
98                Local anesthetics (LAs) block voltage-gated Na+ channels in excitable cells, whereas b
99 udy the role of Na+-dependent exchangers and voltage-gated Na+ channels in the maintenance of membran
100                                         Most voltage-gated Na(+) channels inactivate almost completel
101                                              Voltage-gated Na(+) channels initiate action potentials
102                                              Voltage-gated Na(+) channels initiate and propagate acti
103                                The rat brain voltage-gated Na+ channel is composed of three glycoprot
104                        The inner pore of the voltage-gated Na+ channel is predicted by the structure
105 etter understand why sensory neurons express voltage-gated Na+ channel isoforms that are different fr
106 hat residue with lysine (normally present in voltage-gated Na(+) channels) makes the channel more sel
107                                Inhibition of voltage-gated Na+ channels may contribute to the presyna
108 lar linker between domains III and IV of the voltage-gated Na channel mediates fast inactivation.
109                   Association of beta1B with voltage-gated Na+ channels Na(v)1.1 or Na(v)1.3 is not d
110              In P21 wild-type (WT) rats, the voltage-gated Na+ channels Na(v)1.2, Na(v)1.6, and Na(v)
111                                  Activity of voltage-gated Na channels (Na(v)) is modified by alterna
112 nslational regulation of the primary cardiac voltage-gated Na(+) channel (Na(v)1.5) by Ca(2+)/calmodu
113                               We report that voltage-gated Na+ channels (Na(V)) from rat muscle (mu1)
114               Pancreatic alpha-cells express voltage-gated Na(+) channels (NaChs), which support the
115 he two-pore channel protein family, as a new voltage-gated Na(+) channel (NaV) that generates ulAPs,
116                    Thus, influx of Na(+) via voltage-gated Na(+) channels (NaV ) has emerged as an im
117                                              Voltage-gated Na(+) channels (Nav ) modulate neuronal ex
118       Depolarization leads to the opening of voltage-gated Na(+) channels (Nav) and subsequently volt
119                                              Voltage-gated Na(+) channels (Nav) are essential for myo
120 by de novo gain-of-function mutations in the voltage-gated Na channel Nav1.6.
121 th mutations in the SCN5A gene, encoding the voltage-gated Na(+) channel NaV1.5.
122 (house mice, rats, humans) by activating the voltage-gated Na(+) channel Nav1.7, but has no effect on
123 nction mutations in the human SCN11A-encoded voltage-gated Na(+) channel NaV1.9 cause severe pain dis
124  the mouse gene encoding the skeletal muscle voltage-gated Na+ channel NaV1.4.
125 on after SCI of protein, but not mRNA, for a voltage-gated Na(+) channel, Nav1.8, that is expressed a
126          Neurotransmitter release depends on voltage-gated Na(+) channels (Navs) to propagate an acti
127 duct of action potential generation: (1) the voltage-gated Na(+) channels necessary for action potent
128                                              Voltage-gated Na channels of cerebellar Purkinje neurons
129 n can be classified as beta group toxins for voltage-gated Na+ channels of central neurons.
130 sant drugs acting via use-dependent block of voltage-gated Na(+) channels on GABAergic inhibitory mic
131                                              Voltage-gated Na(+) channels play an essential role in e
132                                        Thus, voltage-gated Na+ channels play cell-autonomous and non
133 ion in ventricular expression of the cardiac voltage-gated Na+ channel pore-forming alpha-subunit (Na
134              Crystal structures of bacterial voltage-gated Na(+) channels predict that the side chain
135 In these neurons, the tetrodotoxin-sensitive voltage-gated Na(+) channels responsible for action pote
136                         The beta subunits of voltage-gated Na channels (Scnxb) regulate the gating of
137 rotons are potent physiological modifiers of voltage-gated Na(+) channels, shifting the voltage range
138  that requires opening of CaV(2.3) channels, voltage-gated Na channels, small conductance Ca-activate
139               Neurons have high densities of voltage-gated Na(+) channels that are restricted to axon
140 te that mossy fiber boutons have specialized voltage-gated Na(+) channels that critically impact upon
141 nel alpha-subunit, have been shown to encode voltage-gated Na+ channels that reopen during prolonged
142 y of several crystal structures of bacterial voltage-gated Na(+) channels, the structure of eukaryoti
143 t alter the expression of different nodal of voltage-gated Na+ channels; the absence of paranodes res
144 blocked by glutamate receptor antagonists, a voltage-gated Na(+) channel toxin, extracellular Ca(2+)
145                                              Voltage-gated Na+ channels undergo two types of inactiva
146   In metazoans, the coordinate activities of voltage-gated Na(+) channels underlie cellular excitabil
147                                              Voltage-gated Na(+) channels underlie rapid conduction i
148 t only by the properties of the pore-forming voltage-gated Na(+) channel (VGSC) alpha subunit, but al
149                                              Voltage-gated Na(+) channel (VGSC) beta1 subunits regula
150                                              Voltage-gated Na(+) channel (VGSC) beta1 subunits, encod
151                         Here we identified a voltage-gated Na(+) channel (VGSC) that was essential fo
152                                              Voltage-gated Na(+) channels (VGSC) have been implicated
153 t only by the properties of the pore-forming voltage-gated Na+ channel (VGSC) alpha subunit, but also
154 ion of the PC-3M cells (24 or 48 h) with the voltage-gated Na+ channel (VGSC) blocker tetrodotoxin (T
155                                              Voltage-gated Na(+) channels (VGSCs) are responsible for
156                We have shown previously that voltage-gated Na(+) channels (VGSCs) are up-regulated in
157                     Functional expression of voltage-gated Na(+) channels (VGSCs) has been demonstrat
158 nt (TTX-R) Na(+) current (I(Na)) mediated by voltage-gated Na(+) channels (VGSCs).
159 raction of symmetrical lidocaine dimers with voltage-gated Na+ channels (VGSCs) was examined using a
160                                    Mammalian voltage-gated Na(+) channels were less sensitive to pyre
161 tial waveforms and gating of less sialylated voltage-gated Na+ channels were altered consistently in
162 the transmembrane segment S6 in domain IV of voltage-gated Na+ channels, whereas the putative BTX rec
163 interaction between the Sig1R and the Nav1.5 voltage-gated Na(+) channel, which has also been implica
164 ert potent use-dependent blocking effects on voltage-gated Na(+) channels, which are thought to under

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