ライフサイエンスコーパス: carbonyl cyanide m-chlorophenylhydrazone

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1 ol ROS bursts after high-dose treatment with carbonyl cyanide m-chlorophenylhydrazone.

2 ed through the addition of the protonophore, carbonyl cyanide m-chlorophenylhydrazone.

3 with a mitochondrial Ca2+ uptake inhibitor, carbonyl cyanide m-chlorophenylhydrazone.

4 ivity was inhibited by the proton ionophores carbonyl cyanide m-chlorophenylhydrazone, 2,4-dinitrophe

5 cold (50% at 4 degrees C), by protonophores (carbonyl cyanide m-chlorophenylhydrazone, 44%, and 2,4-d

6 , an uncoupler of oxidative phosphorylation (carbonyl cyanide m-chlorophenylhydrazone), a superoxide

7 in HIV-1 infectivity was observed only with carbonyl cyanide m-chlorophenylhydrazone, a compound whi

8 e of a membrane potential since inclusion of carbonyl cyanide m-chlorophenylhydrazone, a protonophore

9 Fbxl7 protects mitochondria from actions of carbonyl cyanide m-chlorophenylhydrazone, an inhibitor o

10 Extended pretreatment of B cells with carbonyl cyanide m-chlorophenylhydrazone, an inhibitor o

11 lusion of mitochondrial inhibitors (2 microM carbonyl cyanide m-chlorophenylhydrazone and 2 microM ol

12 Cu-Mb is inhibited by the uncoupling agents carbonyl cyanide m-chlorophenylhydrazone and methylamine

13 B. pertussis strains that were treated with carbonyl cyanide m-chlorophenylhydrazone and sodium arse

14 t and was unaffected by the uncouplers CCCP (carbonyl cyanide m-chlorophenylhydrazone) and DNP (2,4-d

15 Since protonophores CCCP (carbonyl cyanide m-chlorophenylhydrazone) and DTHB (3,5-

16 ligands of the EmrAB pump-2,4-dinitrophenol, carbonyl cyanide m-chlorophenylhydrazone, and carbonyl c

17 uch as rotenone, thenoyltrifluoroacetone, or carbonyl cyanide m-chlorophenylhydrazone, associated wit

18 lectrochemical gradient by the protonophore, carbonyl cyanide m-chlorophenylhydrazone (CCCP) almost c

19 onditions, hypersensitivity to the uncoupler carbonyl cyanide m-chlorophenylhydrazone (CCCP) and mtDN

20 The uncoupler carbonyl cyanide m-chlorophenylhydrazone (CCCP) inhibite

21 h prolonged by mitochondrial inhibition with carbonyl cyanide m-chlorophenylhydrazone (CCCP) or Ruthe

22 model of mitophagy induced by an uncoupler, carbonyl cyanide m-chlorophenylhydrazone (CCCP) that Par

23 When carbonyl cyanide m-chlorophenylhydrazone (CCCP) was appl

24 of murine embryonic fibroblasts treated with carbonyl cyanide m-chlorophenylhydrazone (CCCP), a mitoc

25 ial electron transport chain complex II, and carbonyl cyanide m-chlorophenylhydrazone (CCCP), an unco

26 Driving-ion studies with phenamil, carbonyl cyanide m-chlorophenylhydrazone (CCCP), and dif

27 etween ST1710 and three ligands, salicylate, carbonyl cyanide m-chlorophenylhydrazone (CCCP), and eth

28 Gramicidin and carbonyl cyanide m-chlorophenylhydrazone (CCCP), antimic

29 itochondrial metabolic inhibitors, including carbonyl cyanide m-chlorophenylhydrazone (CCCP), antimyc

30 f the inhibitor of oxidative phosphorylation carbonyl cyanide m-chlorophenylhydrazone (CCCP), dinitro

31 After mitochondrial depolarization with carbonyl cyanide m-chlorophenylhydrazone (CCCP), Flag-gp

32 ssic uncoupler of oxidative phosphorylation, carbonyl cyanide m-chlorophenylhydrazone (CCCP), induced

33 ry, provoked by incubation of platelets with carbonyl cyanide m-chlorophenylhydrazone (CCCP), led to

34 Rotenone, thenoyltrifluoroacetone (TTFA), carbonyl cyanide m-chlorophenylhydrazone (CCCP), Mn(III)

35 gy) stimulated by a mitochondrial uncoupler, carbonyl cyanide m-chlorophenylhydrazone (CCCP), require

36 tivation due to the addition of protonophore carbonyl cyanide m-chlorophenylhydrazone (CCCP), which d

37 l store was estimated by releasing them with carbonyl cyanide m-chlorophenylhydrazone (CCCP).

38 estimated by counting the quanta released by carbonyl cyanide m-chlorophenylhydrazone (CCCP).

39 taneous nerve muscle preparations exposed to carbonyl cyanide m-chlorophenylhydrazone (CCCP, 2 M), ol

40 Depolarizing mitochondria with carbonyl cyanide m-chlorophenylhydrazone (CCCP, 5 microM

41 g, was blocked by pretreatment with azide or carbonyl cyanide m-chlorophenylhydrazone; however, 10% o

42 We found that in the absence of Parkin, carbonyl cyanide m-chlorophenylhydrazone induced the for

43 The electron transport uncoupler carbonyl cyanide m-chlorophenylhydrazone inhibited aceta

44 or treatment with a mitochondrial ionophore, carbonyl cyanide m-chlorophenylhydrazone, initiates a st

45 netic stress) and control cells treated with carbonyl cyanide m-chlorophenylhydrazone (metabolic stre

46 Loading of this store is prevented by carbonyl cyanide m-chlorophenylhydrazone or by antimycin

47 and release (tetraphenylphosphonium or TPP+, carbonyl cyanide m-chlorophenylhydrazone or CCCP, and ru

48 al sequence, was detected in the presence of carbonyl cyanide m-chlorophenylhydrazone or sodium azide

49 In the presence of the uncouplers carbonyl cyanide m-chlorophenylhydrazone or valinomycin,

50 tors of oxidative phosphorylation antimycin, carbonyl cyanide m-chlorophenylhydrazone, or oligomycin.

51 ld-type cells poisoned with the protonophore carbonyl cyanide-m-chlorophenylhydrazone retained their

52 tion rates in both cell lines, whereas CCCP (carbonyl cyanide m-chlorophenylhydrazone) stimulated the

53 translocation to mitochondria in response to carbonyl cyanide m-chlorophenylhydrazone treatment.

54 brid motor was inhibited by the protonophore carbonyl cyanide m-chlorophenylhydrazone under neutral a

55 pumping into reticular stores), and 2 microM carbonyl cyanide m-chlorophenylhydrazone (uptake into mi

56 By using carbonyl cyanide m-chlorophenylhydrazone, we showed that

57 ent and strongly stimulated by the uncoupler carbonyl cyanide m-chlorophenylhydrazone when no externa

58 Unlike the protonophore carbonyl cyanide m-chlorophenylhydrazone, which activate

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