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1 LNPs as well as in the presence of MG132 and concanamycin A.
2 pe cells treated with the V-ATPase inhibitor concanamycin A.
3 lsed targets, and the lysis was inhibited by concanamycin A.
4 ules had been destroyed by pretreatment with Concanamycin A.
5 mediated by perforin and could be blocked by concanamycin A.
6 d sensitivity to nanomolar concentrations of concanamycin A.
7 pe cells treated with the V-ATPase inhibitor concanamycin A.
8  such as ethylene-glyco-tetra-acetic acid or concanamycin A.
9 presence of the specific V-ATPase inhibitor, concanamycin A.
10 e reversed by subnanomolar concentrations of concanamycin A (1), a well-known inhibitor of vacuolar A
11  and unaffected by bafilomycin A(1) (40 nM), concanamycin A (5 nM), sodium o-vanadate (500 microM), o
12 markedly diminished by ammonium chloride and concanamycin A, a selective inhibitor of vacuolar H+ ATP
13 n the vacuolar lumen, V-ATPase inhibition by concanamycin A alkalinized the vacuole and increased BCE
14 e (V-ATPase) inhibitors bafilomycin A(1) and concanamycin A also decreased activation in a concentrat
15 inhibitors such as caffeine, flufenacet, and concanamycin A and (2) across kingdoms with a comparison
16 tment with the vacuolar H+-ATPase inhibitors concanamycin A and bafilomycin A1 or the lysosomotropic
17 monensin or the specific V-ATPase inhibitors concanamycin A and bafilomycin A1 supported a role for V
18                   Cytolysis was abrogated by concanamycin A and EGTA but not brefeldin A or anti-Fas
19                        Although sensitive to concanamycin A and ethyleneglycotetraacetic acid, which
20 s of endosomal acidification bafilomycin A1, concanamycin A, and monensin each lowered virus entry by
21 mpletely inhibited by treatment with EGTA or concanamycin A, and this killing is sensitive to PMSF in
22 Pase (V-ATPase) inhibitors Bafilomycin A1 or Concanamycin A at the 32-cell stage.
23              Further, the perforin inhibitor concanamycin A blocks autologous monocyte killing by CD4
24 f extracellular calcium or by treatment with concanamycin A but was only modestly affected by treatme
25 hrough the perforin-mediated pathway because Concanamycin A, but not Brefeldin A-the selective inhibi
26 ls with the lysosome acidification inhibitor concanamycin A, but not treatment with the proteasome in
27                                              Concanamycin A (CCA), a specific inhibitor of vacuolar A
28                                              Concanamycin A (CMA) counteracted Nef at subnanomolar co
29 ocation process by pretreating cultures with concanamycin A (Con A) prevents cleavage of SNAP-25 with
30 retreatment of target cells with amantadine, concanamycin A, concanamycin B, chloroquine, and ammoniu
31 , methyl-beta-cyclodextrin, chloroquine, and concanamycin A dramatically reduced SHFV entry efficienc
32 vity of the preparation is >95% sensitive to concanamycin A, indicating that the lipid nanodisc-recon
33 a mutant, and acute V-ATPase inhibition with concanamycin A induced coordinate up-regulation from bot
34 e in the same category of bafilomycin A1 and concanamycin A, inhibitors of the vacuolar H(+)-ATPase,
35                           Bafilomycin A1 and concanamycin A, inhibitors of vacuolar ATPases, prevente
36 tant cells with monensin, bafilomycin A1, or concanamycin A is sufficient to change the Adriamycin di
37 ncubation of the cells in ammonium chloride, concanamycin A, leupeptin and E-64.
38  is inhibited in the presence of primaquine, concanamycin A, monensin, cycloheximide, and an inhibito
39                               Treatment with concanamycin A or EGTA abrogated CD8+ NKT cytotoxicity i
40  endosome acidification with bafilomycin A1, concanamycin A, or NH(4)Cl enhanced entry via the fusion
41 resence of a vacuolar H(+)-ATPase inhibitor, concanamycin A, oxidized proteins were detected in the v
42  vacuolar ATPase inhibitor bafilomycin A1 or concanamycin A prior to infection significantly delayed
43 fective V1Vo assembly and a 90% reduction in concanamycin A-sensitive ATPase activity and proton tran
44 loride and thonzonium bromide fully retained concanamycin A-sensitive ATPase activity despite the fac
45 lex, targeting to the vacuolar membrane, and concanamycin A-sensitive ATPase activity.
46 thesis and is associated with an increase in concanamycin A-sensitive proton transport in FITC-loaded
47 idia (asexual spores), and were inhibited by concanamycin, a specific inhibitor of the V-ATPase.
48 s only partially inhibited by either EGTA or concanamycin A, suggesting that these cells use a cytoto
49 ivity, and 5-10 nM bafilomycin A1 or 1-10 nM concanamycin A to inhibit H+-ATPase activity.
50 ced FLS2 endosomal numbers were increased by Concanamycin A treatment but reduced by Wortmannin, indi
51 d but retained at the plasma membrane during concanamycin A treatment.
52   Acute inhibition of V-ATPase activity with concanamycin A triggers Pma1p ubiquitination and interna
53 ent protein-ATG8a fusion in combination with concanamycin A, we also detected the accumulation of aut