ライフサイエンスコーパス: concanamycin

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 sensitive to the specific V-ATPase inhibitor concanamycin.

7 amin (K44A) and a vacuolar-ATPase inhibitor, concanamycin.

8 ockade of the perforin/granzyme pathway with concanamycin.

9 ic vacuolar proton pump (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 and unaffected by bafilomycin A(1) (40 nM), concanamycin A (5 nM), sodium o-vanadate (500 microM), o

14 Concanamycin A (CCA), a specific inhibitor of vacuolar A

15 ocation process by pretreating cultures with concanamycin A (Con A) prevents cleavage of SNAP-25 with

16 n the vacuolar lumen, V-ATPase inhibition by concanamycin A alkalinized the vacuole and increased BCE

17 e (V-ATPase) inhibitors bafilomycin A(1) and concanamycin A also decreased activation in a concentrat

18 inhibitors such as caffeine, flufenacet, and concanamycin A and (2) across kingdoms with a comparison

19 tment with the vacuolar H+-ATPase inhibitors concanamycin A and bafilomycin A1 or the lysosomotropic

20 monensin or the specific V-ATPase inhibitors concanamycin A and bafilomycin A1 supported a role for V

21 Cytolysis was abrogated by concanamycin A and EGTA but not brefeldin A or anti-Fas

22 Although sensitive to concanamycin A and ethyleneglycotetraacetic acid, which

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 , methyl-beta-cyclodextrin, chloroquine, and concanamycin A dramatically reduced SHFV entry efficienc

26 a mutant, and acute V-ATPase inhibition with concanamycin A induced coordinate up-regulation from bot

27 tant cells with monensin, bafilomycin A1, or concanamycin A is sufficient to change the Adriamycin di

28 Treatment with concanamycin A or EGTA abrogated CD8+ NKT cytotoxicity i

29 vacuolar ATPase inhibitor bafilomycin A1 or concanamycin A prior to infection significantly delayed

30 ivity, and 5-10 nM bafilomycin A1 or 1-10 nM concanamycin A to inhibit H+-ATPase activity.

31 ced FLS2 endosomal numbers were increased by Concanamycin A treatment but reduced by Wortmannin, indi

32 d but retained at the plasma membrane during concanamycin A treatment.

33 Acute inhibition of V-ATPase activity with concanamycin A triggers Pma1p ubiquitination and interna

34 markedly diminished by ammonium chloride and concanamycin A, a selective inhibitor of vacuolar H+ ATP

35 s of endosomal acidification bafilomycin A1, concanamycin A, and monensin each lowered virus entry by

36 mpletely inhibited by treatment with EGTA or concanamycin A, and this killing is sensitive to PMSF in

37 hrough the perforin-mediated pathway because Concanamycin A, but not Brefeldin A-the selective inhibi

38 ls with the lysosome acidification inhibitor concanamycin A, but not treatment with the proteasome in

39 retreatment of target cells with amantadine, concanamycin A, concanamycin B, chloroquine, and ammoniu

40 e in the same category of bafilomycin A1 and concanamycin A, inhibitors of the vacuolar H(+)-ATPase,

41 Bafilomycin A1 and concanamycin A, inhibitors of vacuolar ATPases, prevente

42 ncubation of the cells in ammonium chloride, concanamycin A, leupeptin and E-64.

43 is inhibited in the presence of primaquine, concanamycin A, monensin, cycloheximide, and an inhibito

44 endosome acidification with bafilomycin A1, concanamycin A, or NH(4)Cl enhanced entry via the fusion

45 resence of a vacuolar H(+)-ATPase inhibitor, concanamycin A, oxidized proteins were detected in the v

46 s only partially inhibited by either EGTA or concanamycin A, suggesting that these cells use a cytoto

47 ent protein-ATG8a fusion in combination with concanamycin A, we also detected the accumulation of aut

48 fective V1Vo assembly and a 90% reduction in concanamycin A-sensitive ATPase activity and proton tran

49 loride and thonzonium bromide fully retained concanamycin A-sensitive ATPase activity despite the fac

50 lex, targeting to the vacuolar membrane, and concanamycin A-sensitive ATPase activity.

51 thesis and is associated with an increase in concanamycin A-sensitive proton transport in FITC-loaded

52 pe cells treated with the V-ATPase inhibitor concanamycin A.

53 lsed targets, and the lysis was inhibited by concanamycin A.

54 mediated by perforin and could be blocked by concanamycin A.

55 d sensitivity to nanomolar concentrations of concanamycin A.

56 pe cells treated with the V-ATPase inhibitor concanamycin A.

57 such as ethylene-glyco-tetra-acetic acid or concanamycin A.

58 presence of the specific V-ATPase inhibitor, concanamycin A.

59 idia (asexual spores), and were inhibited by concanamycin, a specific inhibitor of the V-ATPase.

60 ed the sensitivity of wild type N. crassa to concanamycin, also proved effective in suppressing the s

61 quenched by nanomolar concentrations of both concanamycin and an indolyl pentadieneamide compound, in

62 inhibits), and transmitter-filled vesicles (concanamycin and bafilomycin inhibit).

63 se activity was also investigated using both concanamycin and inactivating mutations.

64 anzyme B release and the blocking effects of concanamycin and strontium ions.

65 distinguishable from that of the bafilomycin/concanamycin and the salicylihalamide/lobatamide classes

66 Bafilomycin and concanamycin are potent and highly specific inhibitors o

67 Concanamycin B (ConB) and bafilomycin A1 (BFLA1) are spe

68 l appearance, is impaired in the presence of concanamycin B, an inhibitor of vacuolar acidification.

69 arget cells with amantadine, concanamycin A, concanamycin B, chloroquine, and ammonium chloride resul

70 The role of membrane domain subunit a in concanamycin binding and therefore in defining the inhib

71 c, suggesting it forms at least part of the concanamycin binding site.

72 f CCK was decreased by a lysosome inhibitor (concanamycin) but not the proteasome inhibitor lactacyst

73 y were completely resistant to inhibition by concanamycin C, supporting our hypothesis that the V-ATP

74 n and of the plecomacrolides bafilomycin and concanamycin, each coupled to (14)C-labeled 4-(3-trifluo

75 Bafilomycin and concanamycin, highly potent and specific inhibitors of t

76 surprisingly, this activity is both largely concanamycin-insensitive and uncoupled from proton trans

77 The macrolide antibiotic concanamycin is a potent and specific inhibitor of the v

78 h specificity and potency by bafilomycin and concanamycin, macrolide antibiotics with similar structu

79 on, salicylihalamide A does not compete with concanamycin or bafilomycin for binding to V-ATPase, ind

80 Concanamycin partly blocks dissociation of both VCC and

81 either fragment alone and results in higher concanamycin-sensitive ATPase activity and ATP-driven pr

82 mbly is also reflected in a reduced level of concanamycin-sensitive ATPase activity and proton transp

83 of 60-100% of proton transport and 58-93% of concanamycin-sensitive ATPase activity.

84 Pma1p was not mislocalized in concanamycin-treated cells, but a significant reduction

85 toring cytosolic [Ca(2+)] after a pulse than concanamycin-treated wild-type cells, suggesting long te