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1 hat the major target of roscovitine is the P/Q-type calcium channel.
2 dendritic calcium signaling is provided by P/Q-type calcium channels.
3 oding alpha1A, the pore-forming subunit of P/Q-type calcium channels.
4 o both gain- and loss-of-function of human P/Q-type calcium channels.
5 ght to be the pore-forming subunit of P- and Q-type calcium channels.
6 be located near the presynaptic N-type or P/Q-type calcium channels.
7 of fast neurotransmitters relies on N- and P/Q-type calcium channels.
8 d may be secondary to inhibition of N- and P/Q-type calcium channels.
9 ifferences in the inhibition of the N- and P/Q-type calcium channels.
10 The modulation appears to involve N- and P/Q-type calcium channels.
11 fiers in the tightly regulated function of P/Q-type calcium channels.
12 he pore-forming alpha1 subunit of CaV 2.1 (P/Q-type) calcium channels.
13 results suggest a novel processing of the P/Q-type calcium channel and a potential mechanism for the
14 part of this inhibition using recombinant P/Q-type calcium channels and M2 acetylcholine receptors i
15 x via high-voltage-activated (HVA) (N- and P/Q-type) calcium channels and calcium-activated potassium
16 cts in CACNA1A, the alpha1A subunit of the P/Q-type calcium channel, and ataxin-7 (ATXN7), a componen
20 nnel blocker agatoxin IVB, suggesting that P/Q-type calcium channels are the major targets involved i
21 ns in alpha1A, the pore-forming subunit of P/Q-type calcium channels, are linked to several human dis
22 sites, are supported by the activation of P/Q type calcium channels, as opposed to the expected pers
24 Cs was greatly reduced (up to 100%) by the P/Q-type calcium channel blocker agatoxin IVB, suggesting
25 as reduced by 79+/-5% (n=110 cells) by the P/Q-type calcium channel blocker omega-agatoxin-TK (20 nM)
26 aptic calcium influx is through N-type and P/Q-type calcium channels, blocking these channels does no
28 um current (Kir current) and depression of P/Q-type calcium channels by cannabinoids were prevented b
29 vitro function was studied in mice lacking P/Q-type calcium channels (Cav2.1), in which N-type calciu
33 t all vertebrates, including frog, use the P/Q-type calcium channel for neuromuscular transmission.
34 els and the CACNA1A gene, a brain-specific P/Q-type calcium channel gene associated with ataxia and h
36 by N-type calcium channels, whereas L- and P/Q-type calcium channels had little, if any, contribution
37 aptic transmission dependent on N-type and P/Q-type calcium channels is required for stable breathing
39 2 subunit serves in vivo as a component of P/Q-type calcium channels, is indispensable for the centra
40 provide evidence for the hyperactivity of P/Q-type calcium channel-mediated cortical glutamatergic s
41 identifies the developmental importance of P/Q-type calcium channel-mediated presynaptic glutamate re
44 ne of the pore-forming alpha1A subunit for P/Q-type calcium channel, or the CaV3.1 gene of the pore-f
46 oltage-dependent calcium channels, but not P/Q-type calcium channels, prevented the inducible dystoni
47 a bicistronic gene that encodes alpha1A, a P/Q-type calcium channel subunit and a C-terminal protein,
48 mutations (R192Q and S218L) in the CaV2.1 (P/Q-type) calcium channel subunit, pregabalin slowed the s
49 pected association of Ca2+/calmodulin with P/Q-type calcium channels that may contribute to calcium-d
50 the positive effect of roscovitine on the P/Q-type calcium channel, the major mediator of action pot
51 rine cell line causes robust inhibition of P/Q-type calcium channels via pertussis toxin-sensitive G-
52 residual ionic currents were observed when P/Q-type calcium channels were blocked by Cd(2+) or omega-
54 to calcium entry into synaptic boutons via P/Q type calcium channels, whereas asynchronous release is
55 iated by an influx of calcium ions through P/Q-type calcium channels, which are densely localized in
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