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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
10 displacement is blocked upon treatment with xestospongin C, a specific inhibitor of IP(3) receptor a
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
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
21 12 h and was inhibited by ned-19, ryanodine, xestospongin C, and moniliformin, indicating that H(2)O(
23 ,4,5-trisphosphate (IP3) receptor antagonist xestospongin C blocked the cannabinoid effect, suggestin
25 sphate (IP3) receptor antagonists U73122 and xestospongin C, demonstrating involvement of the PLC/IP3
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
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
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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