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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.
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
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
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
24 r proton pump inhibitor, bafilomycin A1, the protonophore carbonyl cyanide m-chorophenylhydrazone or
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
37 nhibiting mitochondrial Ca(2+) uptake by the protonophore CCCP reduced the frequency of GnRH-induced
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
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
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
59 vesicles, GSH is imported via an ATP-driven, protonophore-insensitive, orthovanadate-sensitive mechan
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
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
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
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