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1 thetic compounds to approach the activity of adenophostin A.
4 ), which stimulates production of IP(3), and adenophostin A, a non-hydrolyzable analogue of IP(3).
12 h presumably stimulate production of IP3, or adenophostin A, an IP3R agonist, both induced down-regul
14 In this study, we compared the abilities of adenophostin A and inositol 2,4,5-trisphosphate ((2, 4,5
15 etabolically stable IP(3) receptor agonists, adenophostin A and L-alpha-glycerophospho-D-myoinositol-
16 current study was to compare the effects of adenophostin-A and IP3 on Ca2+ release from stores and C
17 ntraoocyte concentrations of 5-10 microM) of adenophostin-A and IP3 stimulate a large Ca2+ release fr
24 ered to 500 nM, ionomycin, thapsigargin, and adenophostin A did and GPIP(2) and IP(3) did not activat
27 Ins(1,4,5)P3 could still release Ca2+ during adenophostin A-induced Ca2+ influx, confirming that the
28 intracellular Ca2+ buffering (0.1 mM BAPTA), adenophostin A-induced Ca2+ release and activation of Ic
32 n suggested that the novel fungal metabolite adenophostin-A may be able to stimulate Ca2+ entry witho
33 -D-glucopyranoside 2',3, 4-trisphosphate, an adenophostin A mimic lacking most of the adenosine moiet
34 atively open, identifying this region of the adenophostin A molecule as a promising target for furthe
41 e (IP(3)) receptors by the specific agonist, adenophostin A, results in a concentration-dependent dis
43 e suggested that, in likely binding modes of adenophostin A, the area around N(6) may be relatively o
45 lication of inositol 2,4,5-trisphosphate and adenophostin A, two metabolically stable agonists for in
46 h the biological results, docking studies of adenophostin A using the recently reported X-ray crystal
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