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1 sitol 1,4,5-trisphosphate receptor inhibitor Xestospongin C.
2 ented by JNK1/2 siRNA and the IP3R inhibitor xestospongin C.
3 dine, but not by the IP3 receptor antagonist xestospongin C.
4 nd store-mediated Ca2+ entry were blocked by xestospongin C.
5 rs, 2-aminoethoxydiphenyl borate (2-APB) and xestospongin C.
6 sing siRNA or pharmacologic inhibition using xestospongin C.
7 inhibitors 2-aminoethoxyldiphenyl borate and xestospongin-C.
8 kedly attenuated by co-exposure of slices to xestospongin C (1 microM), an antagonist of IP(3) recept
9                   Pretreating cells with (-)-xestospongin C (10 microM) or ryanodine (400 microM), th
10  displacement is blocked upon treatment with xestospongin C, a specific inhibitor of IP(3) receptor a
11                                     However, xestospongin C, a specific inositol 1,4,5-trisphosphate
12                                              Xestospongin C (an inositol 1,4,5-trisphosphate receptor
13 uncovered by application of a combination of xestospongin C, an endoplasmic reticulum inositol 1,4,5-
14 duced increase persisted in cells exposed to xestospongin C, an inhibitor of IP3R-mediated calcium re
15            Consistent with this observation, xestospongin C, an inositol 1,4,5-triphosphate receptor
16                                 In contrast, xestospongin C, an IP3 receptor antagonist, had no effec
17 5-trisphosphate (IP(3)) receptor antagonists xestospongin C and caffeine selectively blocked the seco
18 ffer BAPTA-AM, the IP(3) receptor antagonist Xestospongin C and RNA silencing were used to investigat
19                           Cells treated with xestospongin C and stimulated in the absence of [Ca(2+)]
20 d be initiated in the presence of ryanodine, xestospongin C, and Ca(2+)-free solutions.
21 12 h and was inhibited by ned-19, ryanodine, xestospongin C, and moniliformin, indicating that H(2)O(
22 om thapsigargin, 2 microm 2-APB or 10 microm xestospongin C, and unchanged by PTX.
23 ,4,5-trisphosphate (IP3) receptor antagonist xestospongin C blocked the cannabinoid effect, suggestin
24        The Ca(2+) response was unaffected by xestospongin C but was partially blocked by ryanodine or
25 sphate (IP3) receptor antagonists U73122 and xestospongin C, demonstrating involvement of the PLC/IP3
26 re inhibited by 2-aminoethoxydiphenylborate, xestospongin C, Gd(3+), and La(3+).
27  channel (Gd(3+), 2-APB) and IP(3) receptor (xestospongin C, heparin, 2-APB) blockers.
28  were both attenuated by TRPC3 knockdown and xestospongin C in SR Ca(2+)-depleted arteries.
29 (U73122) or the inositol phosphate receptor (Xestospongin C) inhibited FN-induced elevation of intrac
30 oprotection was blocked by oligomycin and by Xestospongin C, inhibitors of the ATP synthase and of in
31  of calcium channels, ned-19, ryanodine, and xestospongin C, of chloroplasts and mitochondrial electr
32 te (IP(3))-induced Ca(2+) release, 10 microM xestospongin C or 30 microM 2-aminoethoxy-diphenylborate
33 3 receptors with 2 microm 2-APB or 10 microm xestospongin C or by intracellular dialysis of heparin.
34 ect on the secondary Ca2+ response, but when xestospongin C or thapsigargin was loaded into ECs and B
35 5 antagonist (MTEP), IP(3) receptor blocker (xestospongin C), or ROS scavengers (PBN, tempol), but no
36  the inositol 1,4,5-trisphosphate antagonist xestospongin C phenocopy these defects, confirming that
37 nhibition of [Ca2+]i release with heparin or Xestospongin C, prevented the D1-mediated suppression of
38 nositol 1,4,5-trisphosphate receptor blocker xestospongin C resulted in a 37% reduction (199 +/- 25 n
39 lin-1 was inhibited by Ned-19, ryanodine, or xestospongin C, suggesting that NAADP-mediated Ca(2+) si
40               Pretreatment of platelets with Xestospongin C to inhibit IP3-mediated dense tubule calc
41 nositol 1,4,5-triphosphate (IP(3)) receptor, xestospongin-C, we demonstrated that ET-1 induces ER str
42 but were blocked by IP3 receptor antagonists xestospongin-C (Xe-C; 2 microM) or 2-aminoethyl diphenyl
43                                              Xestospongin C (XeC) was shown to selectively block IP(3
44  trisphosphate-mediated calcium release with Xestospongin C (XeC).
45                          2-APB (100 microm), xestospongin C (XeC, 10 microm) or U-73122 (1 microm) bl
46 sphosphate (Ins-1,4,5-P(3)) receptor blocker Xestospongin C (XeC, 2-20 microM) was used to affect [Ca

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