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1 an activity close to that of a commonly used protonophore.
2 (2)-expressing cells with cells exposed to a protonophore.
3 used a decrease of lumenal pH, eliminated by protonophore.
4 ight-induced passive proton flux enhanced by protonophore.
5 ulation, and response of mitochondrial pH to protonophores.
6 d to enable fatty acids to behave as cycling protonophores.
7                                      CCCP (a protonophore; 1 microm) and rotenone (an electron transp
8                            The mitochondrial protonophore 2,4 dinitrophenol (DNP) has beneficial effe
9 osphonium lipophilic cation and releases the protonophore 2,4-dinitrophenol locally in predetermined
10  and reversible activation by the lipophilic protonophore 2-4 dinitrophenol in a pH-dependent manner.
11 ffect on cellular ATP, but rather due to its protonophore activity that leads to cytoplasm acidificat
12 wever, was stimulated about 4-fold by either protonophore and 2-fold by cyanide or increase of pH 7.5
13      From these data, unexpected synergistic protonophore and chitinase inhibition activities have al
14 , and acute 2,4-dinitrophenol (DNP)-treated (protonophore and mitochondrial uncoupler) rats.
15 spermidine uptake and Hst 5 killing, whereas protonophores and cold treatment reduced spermidine upta
16 gy dependent as evidenced by inhibition by a protonophore, and (3) uptake is inhibited by high Zn(II)
17 nsensitive to external pH, pretreatment with protonophores, and treatment with sulfhydryl-modifying r
18 ble expression of mrpA increased the rate of protonophore- and cyanide-sensitive Na+ efflux over that
19 ith the potassium ionophore valinomycin, the protonophore carbonyl cyanide 3-chlorophenylhydrazone, a
20                      It is eliminated by the protonophore carbonyl cyanide m-chlorophenyl hydrazone a
21 r than the activation due to the addition of protonophore carbonyl cyanide m-chlorophenylhydrazone (C
22 aining the hybrid motor was inhibited by the protonophore carbonyl cyanide m-chlorophenylhydrazone un
23                                   Unlike the protonophore carbonyl cyanide m-chlorophenylhydrazone, w
24 r proton pump inhibitor, bafilomycin A1, the protonophore carbonyl cyanide m-chorophenylhydrazone or
25                              Exposure to the protonophore carbonyl cyanide p-(trifluoromethoxy)phenyl
26                                          The protonophore carbonyl cyanide p-(trifluoromethoxy)phenyl
27                             In addition, the protonophore carbonyl cyanide p-trifluoromethoxyphenylhy
28            Wild-type cells poisoned with the protonophore carbonyl cyanide-m-chlorophenylhydrazone re
29 s inhibited by cold (50% at 4 degrees C), by protonophores (carbonyl cyanide m-chlorophenylhydrazone,
30 brane proton electrochemical gradient by the protonophore, carbonyl cyanide m-chlorophenylhydrazone (
31 lux was elicited through the addition of the protonophore, carbonyl cyanide m-chlorophenylhydrazone.
32 d in wild-type meningococci treated with the protonophore carbonylcyanide m-chlorophenylhydrazone (CC
33 of the operon was induced by ethanol and the protonophore carbonylcyanide p-chlorophenylhydrazone (CC
34 K+H+ exchangers respectively, as well as the protonophore carbonylcyanide-m-chlorophenylhydrazone (CC
35 tionary growth phase or cells treated with a protonophore causing a decrease in cellular ATP predomin
36                           Treatment with the protonophore CCCP indicated that only a small percentage
37 nhibiting mitochondrial Ca(2+) uptake by the protonophore CCCP reduced the frequency of GnRH-induced
38        Experiments using both A23187 and the protonophore CCCP revealed that free calcium is absolute
39 rees C, were warmed to 24 degrees C, and the protonophore CCCP was added (20 microM) followed 2 min l
40 trictly dependent on Na(+), resistant to the protonophore CCCP, and sensitive to the sodium ionophore
41 bstrates was prevented by treatment with the protonophore CCCP, with no accompanying decrease in cell
42                                        Since protonophores CCCP (carbonyl cyanide m-chlorophenylhydra
43                                          The protonophore, CCCP markedly inhibited 64Cu incorporation
44 ial membrane depolarization in response to a protonophore, CCCP.
45 ion could be inhibited by NOS antagonists or protonophore collapse of the mitochondrial membrane pote
46 hstanding, titration of low-G cells with low protonophore concentrations, monitoring respiration and
47 d whether a controlled-release mitochondrial protonophore (CRMP) that produces mild liver-targeted mi
48 l pH or pretreatment of the yeast cells with protonophores did not significantly affect the rate of 1
49  carbonyl cyanide m-chlorophenylhydrazone, a protonophore, dissipated the membrane potential and abol
50 Mg(2+), or low doses of palmitic acid or the protonophore FCCP exacerbated Ca(2+)-induced sustained d
51 he mitochondrial membrane potential with the protonophore FCCP or blocking the mitochondrial Ca(2+) u
52 s, during mitochondrial uncoupling using the protonophore FCCP, and during I-R.
53 tion could be blocked with a low dose of the protonophore FCCP, or the mitochondrial KATP channel ant
54 mediated Na(+) influx and was blocked by the protonophore FCCP, thereby implicating mitochondria as t
55       Similar results were obtained with the protonophore FCCP, which is known to reduce the levels o
56                                  Addition of protonophores had the same effect as ExbD D25N.
57 mitochondrial fission factor), and basal and protonophore-induced mitochondrial fragmentation.
58 se, and is associated with an ATP-dependent, protonophore-insensitive 45Ca2+ uptake activity.
59 vesicles, GSH is imported via an ATP-driven, protonophore-insensitive, orthovanadate-sensitive mechan
60  also affected by high concentrations of the protonophore, m-chlorophenylhydrazone (CCCP).
61 a(2+)-independent activity is seen following protonophore-mediated uncoupling, when uncoupling arises
62 n be released from the ER in the presence of protonophore or proton pump inhibitors which increase th
63 ylanilide scaffold, compounds acting only as protonophores or chitinase inhibitors were identified.
64 contrast to the effects of NO, mitochondrial protonophores produced complete depolarizations of mitoc
65           A controlled-release mitochondrial protonophore reverses hypertriglyceridemia, nonalcoholic
66 at acidic buffer pH, and highly sensitive to protonophores; saturable as a function of TPP concentrat
67 al depolarization, because nanomolar CCCP, a protonophore, similarly depolarized mitochondria, elevat
68  of the viable cells remained near basal and protonophore stimulated respiration to the same extent a
69 pspA could be induced by exposure to CCCP, a protonophore that disrupts PMF.
70                         Furthermore, CCCP, a protonophore that disrupts the proton gradient necessary
71 alled CRMP (controlled-release mitochondrial protonophore), that produces mild hepatic mitochondrial
72  lowered ATP concentration during stress and protonophore treatment-induced clgR-pspA expression, sug
73    CCCP (carbonyl cyanide m-chlorophenyl), a protonophore uncoupler that decreases mitochondrial Ca2+
74  and sucrose accumulation was insensitive to protonophores, was comparable in media differing in pota
75                 As closantel is also a known protonophore, we performed a simple scaffold modulation
76  growth on malate when low concentrations of protonophore were present.
77                            DMP 777 acts as a protonophore with specificity for parietal cell acid-sec

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