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1 ntial reduction in binding the NPQ inhibitor dicyclohexylcarbodiimide.
2 arbonate; and had tolerance to inhibition by dicyclohexylcarbodiimide.
3 osition adjacent to subunit b was blocked by dicyclohexylcarbodiimide.
4 ropyl)-N'-ethylcarbodiimide hydrochloride or dicyclohexylcarbodiimide.
9 red in the presence of the inhibitors azide, dicyclohexylcarbodiimide, and aurovertin to elucidate me
10 hylenediphosphonate and imidodiphosphate, by dicyclohexylcarbodiimide, and by the thiol reagent N-eth
12 Potassium fluoride, imidodiphosphate, N,N'-dicyclohexylcarbodiimide, and N-ethylmaleimide also inhi
14 e-linked thiosulfate reductase and that N,N'-dicyclohexylcarbodiimide blocked thiosulfate reductase a
15 the synthetic strategy are as follows: (1) a dicyclohexylcarbodiimide coupling of D-Ala and L-Thr, fo
16 This acylation sequence is mediated by N,N'-dicyclohexylcarbodiimide (DCC) and 4-dimethylaminopyridi
18 cyclization with trifluoroacetic acid or 1,3-dicyclohexylcarbodiimide (DCC), provide novel, high-yiel
19 ive and for the coupling reactions using 1,3-dicyclohexylcarbodiimide (DCC), yields of 80-95% were ob
23 35), and PsbS from these plants did not bind dicyclohexylcarbodiimide (DCCD), a known inhibitor of qE
24 6, 5, or 4, with or without 100 microM N,N'-dicyclohexylcarbodiimide (DCCD), a specific inhibitor of
25 Glu229 (227-245) of the V-PPase and the N,N'-dicyclohexylcarbodiimide (DCCD)-binding transmembrane al
29 ues by Moffatt oxidation (dimethyl sulfoxide/dicyclohexylcarbodiimide/dichloroacetic acid) or with th
30 o be relatively insensitive to inhibition by dicyclohexylcarbodiimide, indicating loss of productive
32 rifluoromethoxy)phenylhydrazone (FCCP), N,N'-dicyclohexylcarbodiimide, phenamil, amiloride, rifampin,
33 onsistent with a proposed mechanism by which dicyclohexylcarbodiimide prevents a conformational inter
35 Site mutations were introduced at the N,N-dicyclohexylcarbodiimide-reactive residue, Glu-857, to e
37 or growth yield, binding of F1 to membranes, dicyclohexylcarbodiimide sensitivity of ATPase activity,
39 ](2-) reacts with the dehydrating agent N,N'-dicyclohexylcarbodiimide to afford tetrametaphosphate an
40 ed by prior treatment of membranes with N,N'-dicyclohexylcarbodiimide to block proton translocation t
41 are extracted with 5 M urea or treated with dicyclohexylcarbodiimide to inactivate F1/Fo ATPase and
42 bit F(1) or with high concentrations of N,N'-dicyclohexylcarbodiimide to label most c subunits preven
43 TPase activity showed enhanced inhibition by dicyclohexylcarbodiimide, which blocks the helix-2 carbo
44 ndrial ATP synthase inhibitors oligomycin or dicyclohexylcarbodiimide, which resulted in a significan
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