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1 thetic compounds to approach the activity of adenophostin A.
2 nositol 1,4,5-trisphosphate receptor agonist adenophostin A (2), are described.
3          Injection of high concentrations of adenophostin A (250 nM) similarly induced rapidly spread
4 ), which stimulates production of IP(3), and adenophostin A, a non-hydrolyzable analogue of IP(3).
5                                              Adenophostin A, a potent activator of the inositol 1, 4,
6                                              Adenophostin-A, a novel compound isolated from cultures
7                                              Adenophostin A activated Icrac after a significant delay
8                                        Thus, adenophostin A activates Icrac as a consequence of relea
9                                              Adenophostin A (AdA) is a potent agonist of the d-myo-in
10                                     Although adenophostin A (AdA), the most potent agonist of d-myo-i
11 7-sensitive pool within 30 s of 1 micrometer adenophostin A addition.
12 h presumably stimulate production of IP3, or adenophostin A, an IP3R agonist, both induced down-regul
13                 The synthesis of a series of adenophostin A analogues modified at C-6 and C-2 of aden
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 They can be viewed as truncated analogues of adenophostin A and refine understanding of structure-act
17  current study was to compare the effects of adenophostin-A and IP3 on Ca2+ release from stores and C
18 ntraoocyte concentrations of 5-10 microM) of adenophostin-A and IP3 stimulate a large Ca2+ release fr
19                                              Adenophostins A and B, which are metabolic products of t
20         With extremely low concentrations of adenophostin A (approximately 10 pM), stable regions of
21 n, and by the potent IP(3) receptor agonist, adenophostin A, but not by GPIP(2) or IP(3) itself.
22                                              Adenophostin A, by virtue of its high receptor affinity,
23                     These data indicate that adenophostin A can stimulate the influx of Ca2+ across t
24           In contrast, low concentrations of adenophostin-A can stimulate Ca2+ influx without stimula
25 ered to 500 nM, ionomycin, thapsigargin, and adenophostin A did and GPIP(2) and IP(3) did not activat
26               Therefore, it is unlikely that adenophostin-A directly stimulates store-operated Ca2+ c
27                                     IP(3) or adenophostin A failed to release (45)Ca(2+) from microso
28 Ins(1,4,5)P3 could still release Ca2+ during adenophostin A-induced Ca2+ influx, confirming that the
29 intracellular Ca2+ buffering (0.1 mM BAPTA), adenophostin A-induced Ca2+ release and activation of Ic
30 oplasmic calcium restricted to the region of adenophostin A-induced calcium mobilization.
31                                     When the adenophostin A-induced calcium signal was restricted to
32 se to inositol 1,4,5-trisphosphate (IP3) and adenophostin-A injection.
33 n suggested that the novel fungal metabolite adenophostin-A may be able to stimulate Ca2+ entry witho
34 -D-glucopyranoside 2',3, 4-trisphosphate, an adenophostin A mimic lacking most of the adenosine moiet
35 atively open, identifying this region of the adenophostin A molecule as a promising target for furthe
36                                              Adenophostin A possesses the highest known affinity for
37                     The limited diffusion of adenophostin A provides an opportunity to examine calciu
38                               In common with adenophostin A, release of Ca2+ from the intracellular s
39                      In high concentrations, adenophostin A released Ca2+ from Ins(1,4, 5)P3-sensitiv
40                          We hypothesize that adenophostin-A releases Ca2+ from a subpopulation of sto
41           Injection of low concentrations of adenophostin A resulted in calcium signals that spread s
42 e (IP(3)) receptors by the specific agonist, adenophostin A, results in a concentration-dependent dis
43              In low concentrations, however, adenophostin A stimulated Ca2+ influx exclusively.
44 e suggested that, in likely binding modes of adenophostin A, the area around N(6) may be relatively o
45                        The unique ability of adenophostin A to activate Icrac under conditions of low
46 lication of inositol 2,4,5-trisphosphate and adenophostin A, two metabolically stable agonists for in
47 h the biological results, docking studies of adenophostin A using the recently reported X-ray crystal
48                        In the current study, adenophostin A was approximately 50-fold more potent tha