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1 ment with the selective H(+)ATPase inhibitor concanamycin.
2 conferred resistance to both bafilomycin and concanamycin.
3 increased resistance to both bafilomycin and concanamycin.
4 o bafilomycin but little or no resistance to concanamycin.
5 utant enzymes showed only weak resistance to concanamycin.
6 amin (K44A) and a vacuolar-ATPase inhibitor, concanamycin.
7 ockade of the perforin/granzyme pathway with concanamycin.
8 ic vacuolar proton pump (v-ATPase) inhibitor concanamycin.
9 sensitive to the specific V-ATPase inhibitor concanamycin.
10 Only the N725F mutation displayed a K(i) for concanamycin (0.84 +/- 0.04 nm) that was slightly higher
11           The lysosomal Ca2+-depleting agent concanamycin (1 mum) enhanced HPV if applied during hypo
12                    vATPase inhibition, using concanamycin (100 nmol/L), blocked the low pHe effects o
13 e reversed by subnanomolar concentrations of concanamycin A (1), a well-known inhibitor of vacuolar A
14  and unaffected by bafilomycin A(1) (40 nM), concanamycin A (5 nM), sodium o-vanadate (500 microM), o
15                                              Concanamycin A (CCA), a specific inhibitor of vacuolar A
16                                              Concanamycin A (CMA) counteracted Nef at subnanomolar co
17 ocation process by pretreating cultures with concanamycin A (Con A) prevents cleavage of SNAP-25 with
18 n the vacuolar lumen, V-ATPase inhibition by concanamycin A alkalinized the vacuole and increased BCE
19 e (V-ATPase) inhibitors bafilomycin A(1) and concanamycin A also decreased activation in a concentrat
20 inhibitors such as caffeine, flufenacet, and concanamycin A and (2) across kingdoms with a comparison
21 tment with the vacuolar H+-ATPase inhibitors concanamycin A and bafilomycin A1 or the lysosomotropic
22 monensin or the specific V-ATPase inhibitors concanamycin A and bafilomycin A1 supported a role for V
23                   Cytolysis was abrogated by concanamycin A and EGTA but not brefeldin A or anti-Fas
24                        Although sensitive to concanamycin A and ethyleneglycotetraacetic acid, which
25 Pase (V-ATPase) inhibitors Bafilomycin A1 or Concanamycin A at the 32-cell stage.
26              Further, the perforin inhibitor concanamycin A blocks autologous monocyte killing by CD4
27 f extracellular calcium or by treatment with concanamycin A but was only modestly affected by treatme
28 , methyl-beta-cyclodextrin, chloroquine, and concanamycin A dramatically reduced SHFV entry efficienc
29 a mutant, and acute V-ATPase inhibition with concanamycin A induced coordinate up-regulation from bot
30 tant cells with monensin, bafilomycin A1, or concanamycin A is sufficient to change the Adriamycin di
31                               Treatment with concanamycin A or EGTA abrogated CD8+ NKT cytotoxicity i
32  vacuolar ATPase inhibitor bafilomycin A1 or concanamycin A prior to infection significantly delayed
33 ivity, and 5-10 nM bafilomycin A1 or 1-10 nM concanamycin A to inhibit H+-ATPase activity.
34 ced FLS2 endosomal numbers were increased by Concanamycin A treatment but reduced by Wortmannin, indi
35 d but retained at the plasma membrane during concanamycin A treatment.
36   Acute inhibition of V-ATPase activity with concanamycin A triggers Pma1p ubiquitination and interna
37 markedly diminished by ammonium chloride and concanamycin A, a selective inhibitor of vacuolar H+ ATP
38 s of endosomal acidification bafilomycin A1, concanamycin A, and monensin each lowered virus entry by
39 mpletely inhibited by treatment with EGTA or concanamycin A, and this killing is sensitive to PMSF in
40 hrough the perforin-mediated pathway because Concanamycin A, but not Brefeldin A-the selective inhibi
41 ls with the lysosome acidification inhibitor concanamycin A, but not treatment with the proteasome in
42 retreatment of target cells with amantadine, concanamycin A, concanamycin B, chloroquine, and ammoniu
43 vity of the preparation is >95% sensitive to concanamycin A, indicating that the lipid nanodisc-recon
44 e in the same category of bafilomycin A1 and concanamycin A, inhibitors of the vacuolar H(+)-ATPase,
45                           Bafilomycin A1 and concanamycin A, inhibitors of vacuolar ATPases, prevente
46 ncubation of the cells in ammonium chloride, concanamycin A, leupeptin and E-64.
47  is inhibited in the presence of primaquine, concanamycin A, monensin, cycloheximide, and an inhibito
48  endosome acidification with bafilomycin A1, concanamycin A, or NH(4)Cl enhanced entry via the fusion
49 resence of a vacuolar H(+)-ATPase inhibitor, concanamycin A, oxidized proteins were detected in the v
50 s only partially inhibited by either EGTA or concanamycin A, suggesting that these cells use a cytoto
51 ent protein-ATG8a fusion in combination with concanamycin A, we also detected the accumulation of aut
52 fective V1Vo assembly and a 90% reduction in concanamycin A-sensitive ATPase activity and proton tran
53 loride and thonzonium bromide fully retained concanamycin A-sensitive ATPase activity despite the fac
54 lex, targeting to the vacuolar membrane, and concanamycin A-sensitive ATPase activity.
55 thesis and is associated with an increase in concanamycin A-sensitive proton transport in FITC-loaded
56 LNPs as well as in the presence of MG132 and concanamycin A.
57 ules had been destroyed by pretreatment with Concanamycin A.
58 pe cells treated with the V-ATPase inhibitor concanamycin A.
59 lsed targets, and the lysis was inhibited by concanamycin A.
60 mediated by perforin and could be blocked by concanamycin A.
61 d sensitivity to nanomolar concentrations of concanamycin A.
62 pe cells treated with the V-ATPase inhibitor concanamycin A.
63  such as ethylene-glyco-tetra-acetic acid or concanamycin A.
64 presence of the specific V-ATPase inhibitor, concanamycin A.
65 idia (asexual spores), and were inhibited by concanamycin, a specific inhibitor of the V-ATPase.
66 ed the sensitivity of wild type N. crassa to concanamycin, also proved effective in suppressing the s
67 quenched by nanomolar concentrations of both concanamycin and an indolyl pentadieneamide compound, in
68  inhibits), and transmitter-filled vesicles (concanamycin and bafilomycin inhibit).
69 se activity was also investigated using both concanamycin and inactivating mutations.
70 anzyme B release and the blocking effects of concanamycin and strontium ions.
71 distinguishable from that of the bafilomycin/concanamycin and the salicylihalamide/lobatamide classes
72  that the most potent compounds were natural concanamycins and their derivatives.
73                              Bafilomycin and concanamycin are potent and highly specific inhibitors o
74                                              Concanamycin B (ConB) and bafilomycin A1 (BFLA1) are spe
75 l appearance, is impaired in the presence of concanamycin B, an inhibitor of vacuolar acidification.
76 arget cells with amantadine, concanamycin A, concanamycin B, chloroquine, and ammonium chloride resul
77     The role of membrane domain subunit a in concanamycin binding and therefore in defining the inhib
78  c, suggesting it forms at least part of the concanamycin binding site.
79 f CCK was decreased by a lysosome inhibitor (concanamycin) but not the proteasome inhibitor lactacyst
80 y were completely resistant to inhibition by concanamycin C, supporting our hypothesis that the V-ATP
81 n and of the plecomacrolides bafilomycin and concanamycin, each coupled to (14)C-labeled 4-(3-trifluo
82                              Bafilomycin and concanamycin, highly potent and specific inhibitors of t
83  surprisingly, this activity is both largely concanamycin-insensitive and uncoupled from proton trans
84                     The macrolide antibiotic concanamycin is a potent and specific inhibitor of the v
85 h specificity and potency by bafilomycin and concanamycin, macrolide antibiotics with similar structu
86 on, salicylihalamide A does not compete with concanamycin or bafilomycin for binding to V-ATPase, ind
87                                              Concanamycin partly blocks dissociation of both VCC and
88 mparison against a set of new, semisynthetic concanamycins revealed that substituents at C-8 and acyl
89  either fragment alone and results in higher concanamycin-sensitive ATPase activity and ATP-driven pr
90 mbly is also reflected in a reduced level of concanamycin-sensitive ATPase activity and proton transp
91 of 60-100% of proton transport and 58-93% of concanamycin-sensitive ATPase activity.
92                Pma1p was not mislocalized in concanamycin-treated cells, but a significant reduction
93 toring cytosolic [Ca(2+)] after a pulse than concanamycin-treated wild-type cells, suggesting long te