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1 phenylhydrazone or the ATPase inhibitor N,N'-dicyclohexylcarbodiimide.
2 arbonate; and had tolerance to inhibition by dicyclohexylcarbodiimide.
3 osition adjacent to subunit b was blocked by dicyclohexylcarbodiimide.
4 ntial reduction in binding the NPQ inhibitor dicyclohexylcarbodiimide.
5 ropyl)-N'-ethylcarbodiimide hydrochloride or dicyclohexylcarbodiimide.
6 as suppressed by cyclosporin A (60%) and 1,3-dicyclohexylcarbodiimide (90%).
7 the enzymatic activity was inhibited by N,N'-dicyclohexylcarbodiimide, an agent known to bind ion-tra
8                           We have found that dicyclohexylcarbodiimide, an inhibitor of mitochondrial
9      BODIPY FL and its activating agents 1,3-dicyclohexylcarbodiimide and 4-dimethylaminopyridine wer
10            Inhibitors of ATP synthase (N, N'-dicyclohexylcarbodiimide and oligomycin) and incubation
11 red in the presence of the inhibitors azide, dicyclohexylcarbodiimide, and aurovertin to elucidate me
12 hylenediphosphonate and imidodiphosphate, by dicyclohexylcarbodiimide, and by the thiol reagent N-eth
13                                     Quinine, dicyclohexylcarbodiimide, and Mg(2+), inhibitors of the
14   Potassium fluoride, imidodiphosphate, N,N'-dicyclohexylcarbodiimide, and N-ethylmaleimide also inhi
15 ree hydroxyl of ganciclovir in pyridine with dicyclohexylcarbodiimide as catalyst.
16 e-linked thiosulfate reductase and that N,N'-dicyclohexylcarbodiimide blocked thiosulfate reductase a
17 the synthetic strategy are as follows: (1) a dicyclohexylcarbodiimide coupling of D-Ala and L-Thr, fo
18  This acylation sequence is mediated by N,N'-dicyclohexylcarbodiimide (DCC) and 4-dimethylaminopyridi
19                       The reaction of 1 with dicyclohexylcarbodiimide (DCC) only proceeds to form the
20 cyclization with trifluoroacetic acid or 1,3-dicyclohexylcarbodiimide (DCC), provide novel, high-yiel
21 ive and for the coupling reactions using 1,3-dicyclohexylcarbodiimide (DCC), yields of 80-95% were ob
22                                         N,N'-dicyclohexylcarbodiimide (DCCD) has been reported to inh
23                                         N,N'-dicyclohexylcarbodiimide (DCCD) has been reported to inh
24   Employing the zero-space cross-linker N,N'-dicyclohexylcarbodiimide (DCCD) in combination with LC-M
25      The relationship between the binding of dicyclohexylcarbodiimide (DCCD) to isolated light-harves
26 35), and PsbS from these plants did not bind dicyclohexylcarbodiimide (DCCD), a known inhibitor of qE
27  6, 5, or 4, with or without 100 microM N,N'-dicyclohexylcarbodiimide (DCCD), a specific inhibitor of
28 Glu229 (227-245) of the V-PPase and the N,N'-dicyclohexylcarbodiimide (DCCD)-binding transmembrane al
29 on translocation and is reactive toward N,N'-dicyclohexylcarbodiimide (DCCD).
30 nhibited by the carboxyl activating reagent, dicyclohexylcarbodiimide (DCCD).
31 erichia coli is blocked by the compound N,N'-dicyclohexylcarbodiimide (DCCD, DCC).
32 ues by Moffatt oxidation (dimethyl sulfoxide/dicyclohexylcarbodiimide/dichloroacetic acid) or with th
33 o be relatively insensitive to inhibition by dicyclohexylcarbodiimide, indicating loss of productive
34                                              Dicyclohexylcarbodiimide-inhibited enzyme, with 1% resid
35 rifluoromethoxy)phenylhydrazone (FCCP), N,N'-dicyclohexylcarbodiimide, phenamil, amiloride, rifampin,
36 onsistent with a proposed mechanism by which dicyclohexylcarbodiimide prevents a conformational inter
37      The c subunit was characterized as N,N'-dicyclohexylcarbodiimide reactive.
38    Site mutations were introduced at the N,N-dicyclohexylcarbodiimide-reactive residue, Glu-857, to e
39 o(51) and the Glu(54) mutants were both more dicyclohexylcarbodiimide-sensitive than wild type.
40 or growth yield, binding of F1 to membranes, dicyclohexylcarbodiimide sensitivity of ATPase activity,
41                                              Dicyclohexylcarbodiimide shifted the ratio of catalytic
42 ](2-) reacts with the dehydrating agent N,N'-dicyclohexylcarbodiimide to afford tetrametaphosphate an
43 ed by prior treatment of membranes with N,N'-dicyclohexylcarbodiimide to block proton translocation t
44 ric anhydride, N-hydroxysuccinimide and N,N'-dicyclohexylcarbodiimide to fabricate a functional surfa
45  are extracted with 5 M urea or treated with dicyclohexylcarbodiimide to inactivate F1/Fo ATPase and
46 bit F(1) or with high concentrations of N,N'-dicyclohexylcarbodiimide to label most c subunits preven
47 TPase activity showed enhanced inhibition by dicyclohexylcarbodiimide, which blocks the helix-2 carbo
48 ndrial ATP synthase inhibitors oligomycin or dicyclohexylcarbodiimide, which resulted in a significan