ライフサイエンスコーパス: voltage-operated

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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 Because L-type voltage-operated Ca(2+) channel inhibitors substantially

7 To determine whether L-type voltage-operated Ca(2+) channels (L-VOCCs) are required

8 It is becoming increasingly clear that voltage-operated Ca(2+) channels (VOCCs) play a fundamen

9 Our results indicate that voltage-operated Ca(2+) channels can modulate oligodendr

10 n, we used a conditional knock-out mouse for voltage-operated Ca(2+) channels in oligodendrocyte prog

11 luxes via K(+) channels, Cl(-) channels, and voltage-operated Ca(2+) channels were studied by compari

12 Nifedipine, an inhibitor of voltage-operated Ca(2+) channels, inhibits progesterone-

13 gether, store depletion causes activation of voltage-operated Ca(2+) entry and CCE.

14 rizontal cells without affecting presynaptic voltage-operated Ca(2+) entry.

15 These kinases modulate voltage-operated Ca(2+) uptake in OPCs and participate i

16 This influx of Ca2+ was not affected by the voltage-operated Ca2+ channel (VOCC) antagonists nicardi

17 se in intracellular Ca2+ that was blocked by voltage-operated Ca2+ channel antagonists.

18 The voltage-operated Ca2+ channel blockers nifedipine (1 mum

19 lcineurin (protein phosphatase 2B (PP2B) and voltage-operated Ca2+ channels (VOCCs) in NG108-15 cells

20 Voltage-operated Ca2+ channels and protein kinases are n

21 These studies establish that T-type voltage-operated Ca2+ channels are required for cell cyc

22 The regulation of non-voltage-operated Ca2+ channels in the plasma membrane re

23 reflect clusters of RyRs closely coupled to voltage-operated Ca2+ channels in the sarcolemma.

24 lator (BAPTA) or Cd2+, a specific blocker of voltage-operated Ca2+ channels, abolished the ability of

25 were mostly determined by the activation of voltage-operated Ca2+ channels.

26 ppear to couple to dihydropyridine-sensitive voltage-operated Ca2+ channels.

27 t to elicit a secondary activation of L-type voltage-operated Ca2+ entry.

28 e examined the role of store-, receptor- and voltage-operated Ca2+ influx pathways in rat intrapulmon

29 mutational modification strongly suppresses voltage-operated calcium (Ca(V)1.2) channels while activ

30 induces Ca(2+)i mobilization via the L-type voltage-operated calcium channel and the inositol 1,4,5-

31 erogeneity in the distribution of functional voltage-operated calcium channel subtypes in the neostri

32 of extracellular calcium (Ca(2)(+)), L-type voltage-operated calcium channels (L-VOCCs), Rho kinase

33 Finally, although Ca2+ influx through voltage-operated calcium channels does not appear to con

34 he relative involvement of N-, P- and Q-type voltage-operated calcium channels in the control of stri

35 This suggests a role for voltage-operated calcium channels in the habituation pro

36 mbranes carry neurotransmitter receptors and voltage-operated channels that are still functional, eve

37 We studied the properties of a voltage-operated Na+ conductance in descending vasa rect

38 We conclude that a TTX-sensitive voltage-operated Na+ conductance, with properties simila

39 Therefore, the voltage-operated sparks phenotype is specific to the RyR

40 RyR1-transfected muscle lacked voltage-operated sparks.

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