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1 sion of calcium-handling genes (eg, SERCA2a, L-type calcium channel).
2 e the same G406R replacement in the Ca(V)1.2 L-type calcium channel.
3 smembrane Ca(2+) conductance mediated by the L-type calcium channel.
4 rate cardiac repolarization by inhibition of L-type calcium channel.
5 oding the alpha1- and beta2b-subunits of the L-type calcium channel.
6 ity filter, similar to the EEEE locus of the L-type calcium channel.
7  had mutations in genes encoding the cardiac L-type calcium channel.
8 on proteins that control the function of the L-type calcium channel.
9 he recently identified Lp and Ls subtypes of L-type calcium channel.
10 genes encoding subunits of the voltage-gated L-type calcium channel.
11 antagonist at both the NMDA receptor and the L-type calcium channel.
12 e no known selective antagonists of Ca(V)1.3 L-type calcium channel.
13 e effects accompanying general antagonism of L-type calcium channels.
14    All E2-BSA-FITC binding neurons expressed L-type calcium channels.
15 t of Erk1/2 on synaptic transmission through L-type calcium channels.
16 cytosis by increasing calcium influx through L-type calcium channels.
17 to induce intracellular calcium flux through L-type calcium channels.
18 lso binds a unique subpopulation of Ca(v)1.2 L-type calcium channels.
19 olely attributable to calcium influx through L-type calcium channels.
20 ransients mediated by high-voltage-activated L-type calcium channels.
21  reflecting activation of NMDA receptors and L-type calcium channels.
22 vated by calcium entry predominantly through L-type calcium channels.
23 om MAPCs (MAPC-SMCs) demonstrated functional L-type calcium channels.
24 primarily by blocking high-voltage-activated L-type calcium channels.
25 ane depolarization and calcium entry through L-type calcium channels.
26 s in the BLC express the Ca(v)1.2 subtype of L-type calcium channels.
27 pamine receptors and impaired by blockers of L-type calcium channels.
28 nt APPsalpha, or by pharmacological block of L-type calcium channels.
29 attenuated by inhibiting cyclooxygenase-2 or L-type calcium channels.
30 retreatment decreased subsequent activity of L-type calcium channels.
31 rvival of cultured neurons via activation of L-type calcium channels.
32 expression as strongly as did stimulation of L-type calcium channels.
33 elease is mediated by calcium influx through L-type calcium channels.
34 nel blocker, to eliminate the involvement of L-type calcium channels.
35 may in part be mediated by the activation of L-type calcium channels.
36 entate molecular layer, was not dependent on L-type calcium channels.
37 ux of extracellular Ca2+, presumably through L-type calcium channels.
38 and their activities on cardiac and neuronal L-type calcium channels.
39 xicity is prevented by calcium entry through L-type calcium channels.
40 irectly binds and facilitates the opening of L-type calcium channels.
41 receptors are linked to nifedipine-sensitive L-type calcium channels.
42 extracellular fragment APPsalpha and involve L-type calcium channels.
43 y the secreted APPsalpha-domain and involves L-type calcium channels.
44 harmacologically, CaV1.1e behaves like other L-type calcium channels.
45 mate receptors but blocked by antagonists of L-type calcium channels.
46 ecorated by MG53 in a process coordinated by L-type calcium channels.
47 ite ( approximately 27-130 mum) have reduced L-type calcium channels.
48 A(A) receptors is dependent on activation of L-type calcium channels.
49 y AMPA/NMDA receptor-mediated recruitment of L-type calcium channels.
50 d class of antihypertensive drugs that block L-type calcium channels.
51 t contraction and expression and activity of L-type calcium channels.
52  in part via miR-145-dependent regulation of L-type calcium channels.
53 pression is thought to require activation of L-type calcium channels, a view based primarily on studi
54              In neonatal rat cardiomyocytes, L-type calcium channel accessory beta-subunit gene knock
55 ce capable of mediating the knockdown of the L-type calcium channel accessory beta-subunit gene was i
56    These findings indicate that knockdown of L-type calcium channel accessory beta-subunit is capable
57 hypothesized that genetic suppression of the L-type calcium channel accessory beta-subunit would modu
58 ate receptor activation, but rather requires L-type calcium channel activation and functional gap jun
59   These findings suggest a scenario in which L-type calcium channel activation is a crucial switch fo
60 tradiol (E2) induced rapid Ca(2+) influx via L-type calcium channel activation, which was required fo
61 naptic depolarization sufficient to activate L-type calcium channels, activation of postsynaptic meta
62 ning mechanical stress-induced activation of L-type calcium channel activity are obscure.
63                                              L-type calcium channel activity is critical to afterload
64  potentials presumably results from Ca(V)1.3 L-type calcium channel activity.
65 d as novel contributors to the regulation of L-type calcium channel activity.
66 d as novel contributors to the regulation of L-type calcium channel activity.
67 ggering cell growth in a manner dependent on L-type calcium channel activity.
68                                          The L type calcium channel agonist (+/-)Bay K 8644 has been
69 eproduction of similar behavior with another L type calcium channel agonist, and the protection affor
70 can be provoked by administration of another L type calcium channel agonist, FPL 64176.
71   The known actions of (+/-)Bay K 8644 as an L type calcium channel agonist, the reproduction of simi
72                           Application of the L-type calcium channel agonist Bay K 8644 or activation
73                              Conversely, the L-type calcium channel agonist Bay K8644 induced stereot
74         To further verify the mechanism, the L-type calcium channel agonist FPL 64176 was administere
75 ized by chronic treatment with either of the L-type calcium channel agonists FPL 64176 or Bay K 8644.
76                                Although most L-type calcium channel alpha(1C) subunits isolated from
77 s required for plasma membrane expression of L-type calcium channels alpha 1S (Cav1.1), probably thro
78 for the cardiac isoform of the voltage-gated L-type calcium channel (alpha(1C)) is elevated in colon
79 e 5' flanking region of exon 1b of the human L-type calcium channel alpha1C gene.
80      In situ hybridization demonstrated that L-type calcium channel alpha1C subunit mRNA expression w
81               Voltage-gated CaV1.2 channels (L-type calcium channel alpha1C subunits) are critical me
82  is demonstrated with simulations of a model L-type calcium channel and a mathematical analysis of a
83              Finally, phosphorylation of the L-type calcium channel and phospholamban were found suff
84                            The voltage-gated L-type calcium channel and the functionally linked calci
85 tion of I-2 at S43 appears to be mediated by L-type calcium channels and calcium/calmodulin-dependent
86 arlier reports that the AHNAKs are linked to L-type calcium channels and can be phosphorylated by pro
87  primarily due to the blockade of pancreatic L-type calcium channels and insulin resistance on the ce
88 ked proteins, such as Shank3 and subunits of l-type calcium channels and NMDA receptors, and increase
89 ne NGP1-01, a dual action antagonist at both L-type calcium channels and NMDA receptors, was measured
90  presynaptic silent synapses is dependent on L-type calcium channels and protein kinase A (PKA)/PKC s
91 increases macroscopic inward current through L-type calcium channels and slows activation and deactiv
92 e show that the C. elegans SHN-1/Shank binds L-type calcium channels and that increased and decreased
93  studies demonstrated an association between L-type calcium channels and the sigma-1 receptors.
94 release by two different mechanisms: through L-type calcium channels and through an increase in the p
95 ence of defective current densities for Ik1, l-type calcium channel, and Na(+)/Ca(2+) exchanger.
96 smic reticulum Ca2+-release channel, cardiac L-type calcium channel, and Na+/Ca2+ exchanger.
97 ) is required for normal function of cardiac L-type calcium channels, and its up-regulation is associ
98 sion, culture in NGF reduces the activity of L-type calcium channels, and secondarily, the calcium-se
99 en peroxide microdomain signaling stimulates L-type calcium channels, and that this mechanism strongl
100 acemaker function, including subunits of the L-type calcium channel, Ank2, and Tbx3.
101 describe the first highly selective Ca(V)1.3 L-type calcium channel antagonist and point to a novel t
102 nt study assessed whether treatment with the L-type calcium channel antagonist nimodipine affects the
103 regarding the effect of the well-established L-type calcium channel antagonist nimodipine.
104      Pretreatment of muscle with nifedipine (L-type calcium channel antagonist) marginally decreased
105 s were inhibited by 20 microM nifedipine, an L-type calcium channel antagonist, and 200 nM omega-agat
106  (8), a potent and highly selective Ca(V)1.3 L-type calcium channel antagonist.
107 nist, and the protection afforded by certain L type calcium channel antagonists implicate calcium cha
108 by pretreating the mice with dihydropyridine L type calcium channel antagonists such as nifedipine, n
109 erapamil, D600) and the insensitivity to non-L-type calcium channel antagonists support the conclusio
110 egrees C and found that, at >/=37 degrees C, L-type calcium channels are active at unexpectedly hyper
111                                              L-type calcium channels are Ca(2+) binding proteins of g
112                                     Neuronal L-type calcium channels are essential for regulating act
113                             Higher levels of L-type calcium channels are in somata/proximal dendrites
114                                         CaV1 L-type calcium channels are key to regulating neuronal e
115 e details surrounding the mechanism by which L-type calcium channels are privileged in signaling to C
116 dolinium, or nimodipine, which suggests that L-type calcium channels are significant routes of zinc u
117 eleton as well as the inhibition of at least L-type calcium channels as major reasons for the observe
118 atment with nickel ions, by such blockers of L-type calcium channels as nifedipine, verapamil and dil
119 es and probably influx through voltage-gated L-type calcium channels as well.
120 he plasma membrane sodium calcium exchanger, L-type calcium channels, ATP-sensitive K(+) channels, or
121  of EGFP-VSNL was specific to the actions of L-type calcium channels, because CREB signaling after NM
122   The results are consistent with a model of L-type calcium channel biosynthesis in which there are o
123                               Nimodipine, an L-type calcium channel blocker has been shown to reduce
124                                          The L-type calcium channel blocker nifedipine (1 microM) had
125 -operated calcium entry blocked DIR, but the L-type calcium channel blocker nifedipine did not.
126 (+) (K(ATP)) channel opener diazoxide or the l-type calcium channel blocker nifedipine mimicked the e
127                       In sharp contrast, the L-type calcium channel blocker verapamil markedly decrea
128 sing this assay, we identified fendiline, an L-type calcium channel blocker, as a specific inhibitor
129 mias could be terminated by nitrendipine, an l-type calcium channel blocker, but not by the Na channe
130 ting pattern, we applied the benzothiazepine L-type calcium channel blocker, diltiazem.
131                                          The L-type calcium channel blocker, nifedipine, significantl
132 nd La(3+) but not by Mg(2+) or the classical l-type calcium channel blocker, nitrendipine.
133 ently, diabetic mice with cilnidipine, an N-/L-type calcium channel blocker, showed a reduction in al
134 a group of hearts with diltiazem, a specific L-type calcium channel blocker, to eliminate the involve
135 sodilator responses to ketamine, whereas the L-type calcium-channel blocker had no significant effect
136                             Other classes of L-type calcium channel blockers did not mislocalize K-Ra
137                  First, we observed that the L-type calcium channel blockers nifedipine and verapamil
138                                          The L-type calcium channel blockers nimodipine and nifedipin
139 al neuroprotective role for centrally acting L-type calcium channel blockers of the dihydropyridine c
140     This study was undertaken to investigate L-type calcium channel blockers of the dihydropyridine c
141                          The addition of the L-type calcium channel blockers, 5 microM nifedipine or
142  were calcium spikes, blocked by cadmium and L-type calcium channel blockers.
143 h not only required activation of mGluRs and L-type calcium channels but also was bidirectionally mod
144 group I metabotropic glutamate receptors, or L-type calcium channels, but involves adenosine acting a
145              We found that the activation of L-type calcium channels by 2,5-dimethyl-4-[2-(phenylmeth
146  rapidly reduced the barium currents through L-type calcium channels by approximately 70% and shifted
147 orted by data showing that the activation of L-type calcium channels by BAY-K 8644 was unchanged duri
148                                     Blocking L-type calcium channels by diltiazem (10 microm) signifi
149                   A missense mutation in the L-type calcium channel Ca(V)1.2 leads to LQTS in patient
150 rome is caused by a missense mutation in the L-type calcium channel Ca(v)1.2 that is associated with
151 h one of its ultimate effectors, the class C L-type calcium channel Ca(v)1.2.
152   The link between Ca(2+) influx through the L-type calcium channels Ca(v)1.2 or Ca(v)1.3 and glucose
153 ructure of the skeletal muscle voltage-gated L-type calcium channel (Ca(v)1.1; dihydropyridine recept
154 protein kinase A-mediated phosphorylation of L-type calcium channel (Ca(v)1.2) and phospholamban.
155 xyl-terminal cleavage product of the cardiac L-type calcium channel (Ca(V)1.2) autoregulates expressi
156       The proximal C terminus of the cardiac L-type calcium channel (Ca(V)1.2) contains structural el
157 CT2, amino acids 1596-1692) of human cardiac L-type calcium channel (Ca(V)1.2) have been expressed, r
158                                              L-type calcium channels (Ca(V)1) are involved in diverse
159                         Ca(2+) entry through L-type calcium channels (Ca(V)1.2) is critical in shapin
160 hich encodes the pore-forming subunit of the L-type calcium channel, Ca(v)1.4.
161  channels involved mainly phosphorylation of L-type calcium channels, Ca(2+)-dependent inactivation v
162     Consolidation requires signaling through L-type calcium channels, CaM kinase kinase, and the GluA
163 ight regulation of calcium entry through the L-type calcium channel CaV1.2 ensures optimal excitation
164 1C, the alpha1C subunit of the voltage-gated L-type calcium channel Cav1.2, rank among the most consi
165                                          The L-type calcium channel CaV1.3 constitutes an important c
166  proteins, only otoferlin interacts with the L-type calcium channel Cav1.3, showing a significant dif
167 S resulted from a recurrent, de novo cardiac L-type calcium channel (CaV1.2) mutation, G406R.
168 Calcium influx through the voltage-dependent L-type calcium channel (CaV1.2) rapidly increases in the
169               The activity and expression of L-type calcium channel (Cav1.2), not T-type calcium chan
170 (2+) and alter the properties of the cardiac L-type calcium channel (CaV1.2).
171                                  In neurons, L-type calcium channels (CaV1.2 and CaV1.3) regulate an
172        This study investigated regulation of L-type calcium channels (Cav1.2b) by acetylcholine (ACh)
173          Here, we study recombinant neuronal L-type calcium channels, CaV1.2 and CaV1.3.
174 ect plasma membrane targeting of the class C L-type calcium channel complexes is generated as a resul
175  the membrane targeting of voltage-dependent L-type calcium channel complexes.
176                                     Neuronal L-type calcium channels contribute to dendritic excitabi
177      Thus, selectively antagonizing Ca(V)1.3 L-type calcium channels could provide a means of diminis
178 sely, beta2-AR overexpression did not affect L-type calcium channel current (ICaL) under basal condit
179 SKard cardiomyocytes show hyperactivation of L-type calcium channel current that could not be reverse
180 s a calcium-dependent down-regulation of the L-type calcium channel currents by depolarization.
181  reduction in the amplitude of voltage-gated L-type calcium channel currents in identified retinal bi
182 cal doses, selectively and potently enhances L-type calcium channel currents in isolated rat ventricu
183 50) for nimodipine block of Ca(V)1.3alpha(1) L-type calcium channel currents is 2.7 +/- 0.3 microm, a
184 e neurons from old mice also exhibit smaller L-type calcium channel currents, providing a plausible m
185                 The present study found that L-type calcium channel-dependent LTP in the CA3-CA1 hipp
186        Together, these results show that the L-type calcium channel-dependent survival and NMDA recep
187 the relative contribution of calcium through L-type calcium channels differs.
188 trix, that the engagement of plasma membrane L-type calcium channels during normal autonomous pacemak
189 strate CALI of connexin43 (Cx43) and alpha1C L-type calcium channels, each tagged with one or two sma
190  calcium-activated potassium channels and an L-type calcium channel (electrical resonance).
191 of proteins, gamma(1), is a component of the L-type calcium channel expressed in skeletal muscle.
192                                              L-type calcium channels expressed in the brain are heter
193 segments of Motifs I-IV of the human cardiac L-type calcium channel, expressed in Xenopus oocytes and
194 h muscle, resulted in a similar reduction of L-type calcium channel expression.
195                    Basal and stretch-induced L-type calcium channel expressions were both decreased i
196                          Transcripts for the L-type calcium channel gene CACNA1C were consistently de
197 7 exclusion activity in a RBFOX2-target, the L-type calcium channel gene, Cacna1c.
198                     The predominant class of L-type calcium channels has a Ca(V)1.2 pore-forming subu
199 urthermore, as pharmacological antagonism of L-type calcium channels has been proposed as a potential
200 nt AMPK phosphorylation, while inhibition of L-type calcium channels has no effect.
201 ds was showing the more specific activity on L-type calcium channels, i.e. A7r5 (IC50 = 0.18 +/- 0.02
202          To determine the involvement of the L-type calcium channel in the bursting pattern, we appli
203 a mechanism requiring calcium influx through L-type calcium channels in alphaT3-1 cells and primary r
204 erved role, from fruit flies to mammals, for L-type calcium channels in augmenting motoneuron excitab
205 the present study, we identify a gradient in L-type calcium channels in dendrites of mouse GnRH neuro
206  block of whole cell barium currents through L-type calcium channels in GH4C1 cells show that the com
207 munized mothers exhibited down-regulation of L-type calcium channels in heart.
208 udies attributing an important role to these L-type calcium channels in late onset sporadic Parkinson
209  findings showing that calcium entry through L-type calcium channels in pyramidal cell dendrites in t
210 ts have been used, for example, to implicate L-type calcium channels in the induction of NMDA recepto
211 sed the probability of detecting activity of L-type calcium channels in the T-tubules of ventricular
212 led a significant increase in the density of L-type calcium channels in tottering mouse cerebellum.
213           EGFP-VSNL significantly attenuated L-type calcium channel-induced CREB phosphorylation and
214 pine, an inhibitor of calcium uptake through L-type calcium channels, inhibited the action of NGF on
215 ations but not [Ca(2+)](c) oscillations, and L-type calcium channel inhibition eliminated [Ca(2+)] os
216  restored normal mRNA levels (blocked by the L-type calcium channel inhibitor, nifedipine).
217 on that is responsive to a specific class of L-type calcium channel inhibitors.
218                                          The L-type calcium channel is the major calcium influx pathw
219 hthalmia-associated transcription factor and L-type calcium channels is severely affected.
220                              The activity of L-type calcium channels is tightly coupled to secretion
221 bunit in a well-characterized voltage-gated, L-type calcium channel, is expressed in hair follicle st
222                        Ca(V)1.2, the cardiac L-type calcium channel, is important for excitation and
223 bound to the alpha(1) subunit of the cardiac L-type calcium channel, is required for calcium-dependen
224 equires a specific influx of calcium through L-type calcium channels, JNK activation is independent o
225  that, although the density of intracellular L-type calcium channel labeling remains constant through
226            We have previously shown that the L-type calcium channel (LCC) antagonist nilvadipine redu
227              Elevated calcium influx through L-type calcium channels leads to activation of a pathway
228 eightened stimulation, calcium entry through L-type calcium channels leads to activation of the trans
229       Pharmacological blockade of the N- and L-type calcium channel lessens renal injury in kidney di
230                                              L-type calcium channel (LTCC) and Na(+)/Ca(2+) exchanger
231                                              l-type calcium channel (LTCC) antagonists have been used
232 G)-like APAs frequently have mutations of an L-type calcium channel (LTCC) CaV1.3.
233                      Ca2+ influx through the L-type calcium channel (LTCC) induces Ca2+ release from
234 a critical role for APP in the regulation of L-type calcium channels (LTCC) in GABAergic inhibitory n
235  the expression and distribution profiles of L-type calcium channels (LTCCs) and explored their role
236  neuronal activity in naive rats by engaging L-type calcium channels (LTCCs) and that intra-CeA LTCC
237                         Cav1.3 voltage-gated L-type calcium channels (LTCCs) are part of postsynaptic
238                                  Conversely, L-type calcium channels (LTCCs) become involved in gluta
239                                       CaV1.3 L-type calcium channels (LTCCs) have been a potential ta
240                                              L-type calcium channels (LTCCs) play important roles in
241                                              L-type calcium channels (LTCCs) regulate diverse facets
242                   Distinct subpopulations of L-type calcium channels (LTCCs) with different functiona
243 beta-cell replication in vitro by activating L-type calcium channels (LTCCs).
244 nit [Val-Ser-Asn-Leu (VSNL)] is critical for L-type calcium channels (LTCs) to interact with the sign
245 pha(1) subunit of the cardiac isoform of the L-type calcium channel may be a useful marker of colon c
246                        This suggests that an L-type calcium channel may participate both short- and l
247 52 protein, as well as antibody targeting of L-type calcium channels may be important in the developm
248 o 39% of neurons by P10-P14, suggesting that L-type calcium channels may contribute to retinocollicul
249 ion is the primary defect in tottering mice, L-type calcium channels may contribute to the generation
250 actory bulb expressing TH and tested whether L-type calcium channels mediate the activity-dependent r
251 r brief depolarization, estradiol attenuated L-type calcium channel-mediated CREB phosphorylation.
252 eta triggered mGluR2/3 signaling, decreasing L-type calcium channel-mediated CREB phosphorylation.
253                                              L-type calcium channel mRNA was upregulated.
254 iculum Ca(2+) release channel and DHPR is an L-type calcium channel of exterior membranes (surface me
255 ed the impact of mitochondrial regulation of L-type calcium channels on subcellular calcium and react
256 pha1 subunit expression (also referred to as L-type calcium channels or alpha1S pore-forming subunits
257 neuronal activity and enhanced by disrupting L-type calcium channels or elevating cAMP.
258 , AMPA, and ionomycin but not by agonists of L-type calcium channels or of metabotropic glutamate rec
259                          In skeletal muscle, L-type calcium channels (or dihydropyridine receptors, D
260 little is known about mechanisms that enable L-type calcium channel participation in neurotransmitter
261 rief input train.SIGNIFICANCE STATEMENT CaV1 L-type calcium channels play a key role in regulating th
262                                              L-type calcium channels play only a minor role in basal
263 cium release, and verapamil, an inhibitor of L-type calcium channels, preferentially affects T1 B cel
264 ium chelators or inhibitors of voltage-gated L-type calcium channels prevented mitochondrial degradat
265 relative to littermate controls, and alpha1C L-type calcium channel protein levels were significantly
266 hibitors of advanced glycation end products, L-type calcium channels, protein kinase C, Rho-kinase, a
267  intracellular Ca2+ triggers inactivation of L-type calcium channels, providing negative Ca2+ feedbac
268 ound that clonidine interacts with sodium or L-type calcium channels, reduces calcium influx into neu
269                                              L-type calcium channels regulate a diverse array of cell
270 uge scaffold protein, AHNAK1, interacts with L-type calcium channels, regulates Ca2+ influx, and defe
271 o nucleus signalling, mediated via NMDAR and L-type calcium channels, results in rapid FOXP1 deSUMOyl
272 egulated, whereas the levels of microRNA-29, L-type calcium channel, sarco/endoplasmic reticulum calc
273  calibrated hMSC PS effects on cardiomyocyte L-type calcium channel/sarcoendoplasmic reticulum calciu
274       Accelerated L-currents originated from L-type calcium channels since they were completely block
275 ession and protein levels for calsequestrin, L-type calcium channel, sodium-calcium exchanger, phosph
276  mutation in zebrafish disrupts the alpha1 C L-type calcium channel subunit (C-LTCC).
277 genes ankyrin-3 (ANK3) and voltage-dependent L-type calcium channel subunit beta-3 (CACNB3) as direct
278                                     Ca(v)1.3 L-type calcium channels sustain the pacemaker current, a
279 sarcomere assembly, whereas mutations in the L-type calcium channel that abort calcium entry do not p
280 electrophysiological evidence implicating an L-type calcium channel that modulates glutamate-induced
281                        T-tubules are rich in L-type calcium channels, therefore our work might also p
282 tion mutations in genes encoding the cardiac L-type calcium channel to be associated with a familial
283 kinase Src, and the Calalpha2 subunit of the l-type calcium channel to trigger rapid calcium (Ca(2+))
284  with PDZ domain proteins, are necessary for L-type calcium channels to effectively activate CREB and
285 transgenic mouse with an increased number of L-type calcium channels to identify the role of an incre
286 tective agent by interacting with sodium and L-type calcium channels to reduce the influx of these io
287                        The susceptibility of L-type calcium channels to voltage-dependent facilitatio
288 eration was antagonized by the voltage-gated L-type calcium channel (VGLCC) blocker nifedipine, consi
289                                Voltage-gated L-type calcium channels (VLCC) are distributed widely th
290 ling, which is independent of influx through L-type calcium channels, was not affected by Dicer KO.
291 Because gadolinium can inhibit both SACs and L-type calcium channels, we perfused a group of hearts w
292         Pharmacological agents selective for L-type calcium channels were employed to assess the role
293 antagonists support the conclusion that only L-type calcium channels were present.
294  neurons by enhancing calcium influx through L-type calcium channels, whereas NMDA receptor-mediated
295 ming alpha(1C) subunit of Ca(v)1.2 channels (L-type calcium channels), whose promoter has 2 binding s
296                                              L-type calcium channels with a Ca(V)1.3 pore-forming sub
297              Reducing calcium influx through L-type calcium channels with nicardipine also blocked re
298          Direct activation of alphaT3-1 cell L-type calcium channels with the agonist Bay-K 8644 resu
299 xplained by the interaction of the gating of L-type calcium channels with the changes in driving forc
300           KP4 is shown to specifically block L-type calcium channels with weak voltage dependence to

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