ライフサイエンスコーパス: DEPC

1 DEPC (1 mM) abolished Zn2+-induced inhibition and also t

2 DEPC and [(14)C]DEPC modification, coupled with amino ac

3 DEPC does not affect the absorption spectrum of cytochro

4 DEPC has a primary (18)O isotope effect of 1.041 +/- 0.0

5 DEPC modification indicates that the I state in Na(+)-in

6 DEPC was used to further characterize the inhibition bec

7 he histidines using nonradiolabeled and [14C]DEPC indicates that between one and two histidine residu

8 Plasmin digestion of [14C]DEPC-treated Cp (and N-terminal sequence analysis of the

9 Quantitative [14C]DEPC binding studies indicated the importance of a singl

10 Labeling with [14C]DEPC localized both of these histidyl residues on beta-t

11 yrocarbonate (DEPC) at a mole ratio of 0.74 (DEPC/total His residues) for 3 min at 25 degreesC comple

12 ue, suggesting an active site location for a DEPC target.

13 oth A 5-P and PEP protect the mutant against DEPC inactivation but to different extents from those ob

14 The H97G mutant is protected by PEP against DEPC inactivation to the same degree as the wild-type en

15 The H241G mutant is protected against DEPC inactivation by PEP and A 5-P to the same extent as

16 KDO 8-P synthase is protected against DEPC inactivation by PEP and partially protected against

17 DAH 7-P synthase (Phe) is protected against DEPC inactivation by phosphoenolpyruvate, whereas d-eryt

18 Protection against DEPC inactivation is afforded by a substrate analogue, s

19 on is first order with respect to enzyme and DEPC concentrations with a pseudo-second order rate cons

20 he inactivation is first-order in enzyme and DEPC.

21 fication studies using hydroxyl radicals and DEPC identify nonoverlapping primary binding sites for S

22 llows the rank order POPC/POPG approximately DEPC/DEPG > DPePC/DPePG > DOPC/DOPG.

23 were carried out in explicit lipid bilayers (DEPC, POPC, DMPC, sphingomyelin), confirming the observe

24 at modification of His residues of band 3 by DEPC reduced I- quenching at pH 6.

25 h isoform E subunit are N-carbethoxylated by DEPC.

26 H79 is also derivatized by DEPC at pH 7.0 and above, whereas H62 does not react at

27 4C]UDP-GlcUA uptake rates were diminished by DEPC treatment of intact microsomes, the accumulation of

28 The inhibitory effect by DEPC was significantly protected (90%) by pretreating th

29 sts that the inactivation of heparinase I by DEPC is specific for histidine residues.

30 ts that the inactivation of heparinase II by DEPC is specific for histidine residues and that three h

31 At pH 6.5 wild-type enzyme is inactivated by DEPC after derivatization of one histidine, shown to be

32 econd order rate constant of inactivation by DEPC of 4.9 +/- 0.8 m(-1) s(-1) at pH 6.8 and 4 degrees

33 protects the cytochrome from inactivation by DEPC, indicating that the essential histidine is in the

34 This inhibition by DEPC was also reversed by hydroxylamine.

35 hese two peptides did not become modified by DEPC.

36 ine and lysine residues had been modified by DEPC.

37 es and that three histidines are modified by DEPC.

38 nterestingly, modification of the protein by DEPC was also found to reduce the metal cluster.

39 xyformylation of three histidine residues by DEPC.

40 DEPC and [(14)C]DEPC modification, coupled with amino acid sequencing an

41 Under these conditions DEPC reacts only with histidyl residues.

42 Diethylpyrocarbonate (DEPC) treatment of the protein abolished its binding to

43 at N-3 and G at N-1), diethylpyrocarbonate (DEPC; to probe A at N-7), dimethyl sulfate (DMS; to prob

44 chemically modified by diethylpyrocarbonate (DEPC).

45 information content of diethylpyrocarbonate (DEPC) as a covalent probe of protein surface structure h

46 79A, and the effect of diethylpyrocarbonate (DEPC) have been investigated to elucidate the dehydratas

47 lfonic acid (DIDS), or diethylpyrocarbonate (DEPC).

48 e His-specific reagent diethylpyrocarbonate (DEPC) showed that one or more His residues was specifica

49 l modification reagent diethylpyrocarbonate (DEPC) was used to modify alpha 1-acid glycoprotein (oros

50 dine-modifying reagent diethylpyrocarbonate (DEPC).

51 ibe a method that uses diethylpyrocarbonate (DEPC) labeling and mass spectrometry to detect three-dim

52 as also assessed using diethylpyrocarbonate (DEPC), which modifies histidines.

53 ical modification with diethylpyrocarbonate (DEPC) and site-directed mutagenesis demonstrating the si

54 sidues of tubulin with diethylpyrocarbonate (DEPC) at a mole ratio of 0.74 (DEPC/total His residues)

55 substrate myristoyl-ACP protected HlyC from DEPC inhibition.

56 ate was unable to protect heparinase II from DEPC inactivation for either of the substrates.

57 In H233D, DEPC targets one less histidine than was measured using

58 Importantly, DEPC labeling is able to provide information for up to 3

59 formed from DMPC and for longer channels in DEPC.

60 ysis of O,O-diethylphosphorylcholine iodide (DEPC) and the primary (18)O effect in the alkaline hydro

61 in less than 3 min, and as low as 10 microM DEPC results in a 85% loss of heparinase I activity in 1

62 difying diethyl pyrocarbonate (DEPC); 0.3 mM DEPC results in 95% of heparinase I inactivation in less

63 Moreover, DEPC inactivates cytochrome b(561) more rapidly at alkal

64 ion with heparin followed by the addition of DEPC resulted in a loss of enzymatic activity toward hep

65 ly straightforward mass spectral analysis of DEPC-labeled proteins, we expect this method should be a

66 This result expands the capability of DEPC as a structural probe because about 25% of the sequ

67 The extents of DEPC modification of the histidine and tyrosine residues

68 lity and histidine reactivity information of DEPC-modified OMD necessary for the design of experiment

69 The inherent problem of instability of DEPC-modified histidine residues was overcome by adjusti

70 sary information to describe the reaction of DEPC with OMD.

71 Ferri/ferrocyanide can mediate reduction of DEPC-treated cytochrome b(561) by ascorbic acid, indicat

72 rans DOPC (dielaidoyl phosphatidylcholine or DEPC) on the morphology of giant unilamellar vesicles (G

73 holine/1, 2-dielaidoyl-phosphatidylglycerol (DEPC/DEPG) liposomes at pH 5.0 as a function of peptide

74 d 1,2-dierucoyl-sn-glycero-3-phosphocholine (DEPC).

75 er low specificity of diethyl pyrocarbonate (DEPC) for histidine modification, we modified Tris-washe

76 e histidine-modifying diethyl pyrocarbonate (DEPC) inhibited acyltransferase activity, and acyltransf

77 Treatment with diethyl pyrocarbonate (DEPC) inhibits reduction of the cytochrome by ascorbate,

78 Diethyl pyrocarbonate (DEPC) modification of isoform E nearly abolishes its cyt

79 rcular dichroism, and diethyl pyrocarbonate (DEPC) modification.

80 tein was reacted with diethyl pyrocarbonate (DEPC) over a range of pH values.

81 Diethyl pyrocarbonate (DEPC), a histidine residue-specific reagent, completely

82 hydrophobic reagents [diethyl pyrocarbonate (DEPC), p-bromophenacyl bromide] as compared to the more

83 he) is inactivated by diethyl pyrocarbonate (DEPC).

84 i)) is inactivated by diethyl pyrocarbonate (DEPC).

85 e histidine-modifying diethyl pyrocarbonate (DEPC); 0.3 mM DEPC results in 95% of heparinase I inacti

86 ase is inactivated by diethyl pyrocarbonate (DEPC); activity can be fully restored by incubation with

87 Diethyl pyrocarbonate (DEPC; 10 mM) treatment of P2X4-injected oocytes had no e

88 ormone as model systems, we demonstrate that DEPC labeling can identify both specific protein regions

89 ome b(561) by ascorbic acid, indicating that DEPC-inhibited cytochrome b(561) cannot accept electrons

90 Further evidence for this is that DEPC treatment inhibits oxidation of the cytochrome by s

91 tems, we demonstrate for the first time that DEPC can modify Ser and Thr residues in addition to His

92 The DEPC modification was pH dependent and reversible by hyd

93 Although the DEPC--MMOB species exhibited only minor changes relative

94 Given the simplicity of the DEPC labeling chemistry and the relatively straightforwa

95 ent of wild-type lyase His-233 as one of the DEPC targets.

96 f oxidants and reductants and removal of the DEPC-histidine adduct by sodium hydroxide.

97 Characterization of the DEPC-modified Rieske protein, which remains redox active

98 8-P synthase activity is not restored to the DEPC-inactivated enzyme following treatment with hydroxy

99 ds showed that decreasing bilayer thickness (DEPC-POPC-DMPC) led to an increase in the helix tilt ang

100 These mutants were also subjected to DEPC modification, and results are consistent with the p

101 Finally, when DEPC modification of the protein was carried out in the

102 Double-modification experiments with DEPC and Pt-TP demonstrate that both modifiers affect th

103 Similarly, tubulin modification with DEPC for longer times (8 min) resulted in complete inhib

104 Experiments involving modification with DEPC suggest that a histidine is essential and is protec