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1 pe cells treated with the V-ATPase inhibitor concanamycin A.
2 lsed targets, and the lysis was inhibited by concanamycin A.
3 mediated by perforin and could be blocked by concanamycin A.
4 d sensitivity to nanomolar concentrations of concanamycin A.
5 pe cells treated with the V-ATPase inhibitor concanamycin A.
6 such as ethylene-glyco-tetra-acetic acid or concanamycin A.
7 presence of the specific V-ATPase inhibitor, concanamycin A.
8 and unaffected by bafilomycin A(1) (40 nM), concanamycin A (5 nM), sodium o-vanadate (500 microM), o
9 markedly diminished by ammonium chloride and concanamycin A, a selective inhibitor of vacuolar H+ ATP
10 n the vacuolar lumen, V-ATPase inhibition by concanamycin A alkalinized the vacuole and increased BCE
11 e (V-ATPase) inhibitors bafilomycin A(1) and concanamycin A also decreased activation in a concentrat
12 inhibitors such as caffeine, flufenacet, and concanamycin A and (2) across kingdoms with a comparison
13 tment with the vacuolar H+-ATPase inhibitors concanamycin A and bafilomycin A1 or the lysosomotropic
14 monensin or the specific V-ATPase inhibitors concanamycin A and bafilomycin A1 supported a role for V
17 s of endosomal acidification bafilomycin A1, concanamycin A, and monensin each lowered virus entry by
18 mpletely inhibited by treatment with EGTA or concanamycin A, and this killing is sensitive to PMSF in
20 f extracellular calcium or by treatment with concanamycin A but was only modestly affected by treatme
21 hrough the perforin-mediated pathway because Concanamycin A, but not Brefeldin A-the selective inhibi
22 ls with the lysosome acidification inhibitor concanamycin A, but not treatment with the proteasome in
24 ocation process by pretreating cultures with concanamycin A (Con A) prevents cleavage of SNAP-25 with
25 retreatment of target cells with amantadine, concanamycin A, concanamycin B, chloroquine, and ammoniu
26 , methyl-beta-cyclodextrin, chloroquine, and concanamycin A dramatically reduced SHFV entry efficienc
27 a mutant, and acute V-ATPase inhibition with concanamycin A induced coordinate up-regulation from bot
28 e in the same category of bafilomycin A1 and concanamycin A, inhibitors of the vacuolar H(+)-ATPase,
30 tant cells with monensin, bafilomycin A1, or concanamycin A is sufficient to change the Adriamycin di
32 is inhibited in the presence of primaquine, concanamycin A, monensin, cycloheximide, and an inhibito
34 endosome acidification with bafilomycin A1, concanamycin A, or NH(4)Cl enhanced entry via the fusion
35 resence of a vacuolar H(+)-ATPase inhibitor, concanamycin A, oxidized proteins were detected in the v
36 vacuolar ATPase inhibitor bafilomycin A1 or concanamycin A prior to infection significantly delayed
37 fective V1Vo assembly and a 90% reduction in concanamycin A-sensitive ATPase activity and proton tran
38 loride and thonzonium bromide fully retained concanamycin A-sensitive ATPase activity despite the fac
40 thesis and is associated with an increase in concanamycin A-sensitive proton transport in FITC-loaded
42 s only partially inhibited by either EGTA or concanamycin A, suggesting that these cells use a cytoto
44 ced FLS2 endosomal numbers were increased by Concanamycin A treatment but reduced by Wortmannin, indi
46 Acute inhibition of V-ATPase activity with concanamycin A triggers Pma1p ubiquitination and interna
47 ent protein-ATG8a fusion in combination with concanamycin A, we also detected the accumulation of aut
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