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1 associated with increases in the activity of voltage operated Ca(2+) channels (VOCCs).
2                      These data suggest that voltage operated Ca(2+) channels, mitochondrial Ca(2+) a
3 nal action potentials are mediated solely by voltage-operated Ca(2)(+) channel activation, and slower
4 ght closes cyclic nucleotide-gated (CNG) and voltage-operated Ca(2+) -permeable channels in mammalian
5 terization of the entire family of planarian voltage-operated Ca(2+) channel alpha subunits (Ca(v)alp
6 ed by cytosolic calcium and inhibited by the voltage-operated Ca(2+) channel blocker nifedipine.
7                               Because L-type voltage-operated Ca(2+) channel inhibitors substantially
8                  To determine whether L-type voltage-operated Ca(2+) channels (L-VOCCs) are required
9       It is becoming increasingly clear that voltage-operated Ca(2+) channels (VOCCs) play a fundamen
10                    Our results indicate that voltage-operated Ca(2+) channels can modulate oligodendr
11 n, we used a conditional knock-out mouse for voltage-operated Ca(2+) channels in oligodendrocyte prog
12 luxes via K(+) channels, Cl(-) channels, and voltage-operated Ca(2+) channels were studied by compari
13                  Nifedipine, an inhibitor of voltage-operated Ca(2+) channels, inhibits progesterone-
14 gether, store depletion causes activation of voltage-operated Ca(2+) entry and CCE.
15 rizontal cells without affecting presynaptic voltage-operated Ca(2+) entry.
16                       These kinases modulate voltage-operated Ca(2+) uptake in OPCs and participate i
17  This influx of Ca2+ was not affected by the voltage-operated Ca2+ channel (VOCC) antagonists nicardi
18 se in intracellular Ca2+ that was blocked by voltage-operated Ca2+ channel antagonists.
19                                          The voltage-operated Ca2+ channel blockers nifedipine (1 mum
20 lcineurin (protein phosphatase 2B (PP2B) and voltage-operated Ca2+ channels (VOCCs) in NG108-15 cells
21                                              Voltage-operated Ca2+ channels and protein kinases are n
22          These studies establish that T-type voltage-operated Ca2+ channels are required for cell cyc
23                        The regulation of non-voltage-operated Ca2+ channels in the plasma membrane re
24  reflect clusters of RyRs closely coupled to voltage-operated Ca2+ channels in the sarcolemma.
25 lator (BAPTA) or Cd2+, a specific blocker of voltage-operated Ca2+ channels, abolished the ability of
26  were mostly determined by the activation of voltage-operated Ca2+ channels.
27 ppear to couple to dihydropyridine-sensitive voltage-operated Ca2+ channels.
28 t to elicit a secondary activation of L-type voltage-operated Ca2+ entry.
29 e examined the role of store-, receptor- and voltage-operated Ca2+ influx pathways in rat intrapulmon
30  mutational modification strongly suppresses voltage-operated calcium (Ca(V)1.2) channels while activ
31  induces Ca(2+)i mobilization via the L-type voltage-operated calcium channel and the inositol 1,4,5-
32 erogeneity in the distribution of functional voltage-operated calcium channel subtypes in the neostri
33  of extracellular calcium (Ca(2)(+)), L-type voltage-operated calcium channels (L-VOCCs), Rho kinase
34        Finally, although Ca2+ influx through voltage-operated calcium channels does not appear to con
35 he relative involvement of N-, P- and Q-type voltage-operated calcium channels in the control of stri
36                     This suggests a role for voltage-operated calcium channels in the habituation pro
37 mbranes carry neurotransmitter receptors and voltage-operated channels that are still functional, eve
38               We studied the properties of a voltage-operated Na+ conductance in descending vasa rect
39             We conclude that a TTX-sensitive voltage-operated Na+ conductance, with properties simila
40                               Therefore, the voltage-operated sparks phenotype is specific to the RyR
41               RyR1-transfected muscle lacked voltage-operated sparks.