ライフサイエンスコーパス: sulfhydryl reagent

1 n externally applied and membrane-impermeant sulfhydryl reagent.

2 by p-chloromercuriphenylsulfonate (pCMPS), a sulfhydryl reagent.

3 de of TM3, was affected by membrane-permeant sulfhydryl reagents.

4 ive to vanadate, Ca(2+), and modification by sulfhydryl reagents.

5 nd cumene hydroperoxide, and is inhibited by sulfhydryl reagents.

6 extracellularly applied, membrane-impermeant sulfhydryl reagents.

7 bling its selective chemical modification by sulfhydryl reagents.

8 e residues along the loop with water-soluble sulfhydryl reagents.

9 d aggregation was, however, inhibited by the sulfhydryl reagents.

10 telets were labeled with membrane-impermeant sulfhydryl reagents.

11 d dimers and can be reduced to monomers with sulfhydryl reagents.

12 hibition of the wild-type CTP by hydrophilic sulfhydryl reagents.

13 n the rates of copper uptake and response to sulfhydryl reagents.

14 robed their state-dependent accessibility to sulfhydryl reagents.

15 Cys residues were modified with a bulky sulfhydryl reagent, 1-dimethylaminonaphthalene-5-sulfona

16 Transport by GAT-1 is sensitive to the polar sulfhydryl reagent 2-aminoethyl methanethiosulfonate.

17 e transporter sensitive to inhibition by the sulfhydryl reagents 2-aminoethyl methanethiosulfonate (M

18 d their accessibility to modification by the sulfhydryl reagent 3-(N-maleimido-propionyl) biocytin (M

19 of the introduced cysteine residues with the sulfhydryl reagent 3-(N-maleimidopropionyl)biocytin (bio

20 cid (AMS) followed by the membrane permeable sulfhydryl reagent 3-(N-maleimidylpropionyl) biocytin (M

21 the outer membrane of E. coli, along with a sulfhydryl reagent, 3-(N-maleimidylpropionyl) biocytin (

22 Cys 193 was then modified with a bulky sulfhydryl reagent, 3-(N-maleimidylpropionyl)-biocytin (

23 zan derivative which in turn reacts with the sulfhydryl reagent 4,4'-dithiodipyridine to produce the

24 oups of all mutants reacted rapidly with the sulfhydryl reagent 4,4'-dithiodipyridine, which indicate

25 as sites of attachment of the photoactivated sulfhydryl reagent 4-(N-maleimido)benzophenone (MBP).

26 ing was performed using the photoactivatable sulfhydryl reagent 4-(N-maleimido)benzophenone.

27 in the presence or absence of the impermeant sulfhydryl reagent 4-acetamido-4'-maleimidylstilbene-2,2

28 to react with a large and rigid hydrophilic sulfhydryl reagent, 4-acetamido-4'-[(iodoacetyl)amino]st

29 e incubated with or without a highly charged sulfhydryl reagent, 4-acetamido-4'-maleimidylstilbene-2,

30 mino)ethyl methanethiosulfonate (MTS-TAMRA)) sulfhydryl reagents, 4 with only BM, and 3 with only MTS

31 hione (GSH) involves oxidation of GSH by the sulfhydryl reagent 5,5'-dithio-bis(2-nitrobenzoic acid)

32 reaction rates of cysteine residues with the sulfhydryl reagent 5,5'-dithiobis(2-nitrobenzoic acid) w

33 Cytoplasmically applied membrane-impermeant sulfhydryl reagents alter the Ca2+ sensitivity of Ano1 E

34 Based on the inhibitory effect of sulfhydryl reagents and antibodies, network formation in

35 These multimers could be disaggregated by sulfhydryl reagents and by dimethylmaleic anhydride, and

36 istal from the C terminus) reacted with both sulfhydryl reagents and readily formed disulfide cross-l

37 easily accessible to extracellularly applied sulfhydryl reagents and select for anionic sulfhydryl re

38 ng the SP receptor were treated with various sulfhydryl reagents and the effect of these reagents on

39 ration of 5 S RNA, is extremely sensitive to sulfhydryl reagents and to oxidation, suggesting a role

40 f rat brain tubulin, some react rapidly with sulfhydryl reagents, and some react slowly.

41 stituted P region residues to small, charged sulfhydryl reagents applied to the inside and outside of

42 te their sensitivity to membrane-impermeable sulfhydryl reagents as exchanger current block.

43 (MTSEA(+)) and negatively (pCMBS(-)) charged sulfhydryl reagents, as well as Cd(2+), were added extra

44 Several positively charged sulfhydryl reagents blocked ACh-induced responses for al

45 Modification of yeast actin by a sulfhydryl reagent CPM [7-(diethylamino)-3-(4'-maleimido

46 complex in a manner that is prevented by the sulfhydryl reagents cysteine and dithiothreitol but is n

47 esidue in the propeptide of stromelysin-1 by sulfhydryl reagents did not result in an active enzyme a

48 Cys-5 was modified with the fluorescent sulfhydryl reagent IAANS to probe the conformation of th

49 Sulfhydryl reagents inactivate GPtdIns-PLC, suggesting t

50 Cys122-->Ser permease is insensitive to the sulfhydryl reagent, indicating that NEM inhibition resul

51 The reaction of five of these mutants with sulfhydryl reagents inhibited antagonist binding, and bo

52 sulfhydryl group at beta93Cys is modified by sulfhydryl reagents, iodoacetamide (IAA) and N-ethylmale

53 ated the reaction of the membrane-impermeant sulfhydryl reagent methanethiosulfonate ethyltrimethylam

54 The uncharged sulfhydryl reagent methymethanethiosulfonate (MMTS) did

55 Briefly, the sulfhydryl reagent MTSET was allowed to react, in the pr

56 essibility of introduced Cys residues to the sulfhydryl reagent MTSET.

57 activity and the enzyme was sensitive to the sulfhydryl reagent N-ethylmaleimide (I50, 20 microM).

58 ut transport becomes highly sensitive to the sulfhydryl reagent N-ethylmaleimide (NEM) in a manner si

59 beta-ME-treated membrane is treated with the sulfhydryl reagent N-ethylmaleimide or p-chloromercuribe

60 P/ADP carrier inhibitor atractyloside or the sulfhydryl reagent N-ethylmaleimide.

61 f Cys111 was achieved by the maleimide-based sulfhydryl reagents N-ethylmaleimide (NEM) and fluoresce

62 re measured before and after exposure to the sulfhydryl reagent, N-biotinylaminoethyl methanethiosulf

63 Two sulfhydryl reagents, N-ethylmaleimide (NEM), an alkylati

64 neous or engineered cysteines to small polar sulfhydryl reagents need to be interpreted with extreme

65 The sulfhydryl reagent NEM inhibited the binding of n-sec1 t

66 being the only remaining Cys) indicated that sulfhydryl reagents no longer inhibit but in fact stimul

67 results, the previously observed effects of sulfhydryl reagents on the alternative oxidase of isolat

68 d sulfhydryl reagents and select for anionic sulfhydryl reagents over cationic ones.

69 activity and the effect of the water soluble sulfhydryl reagent p-chloro- mercuribenzenesulfonic acid

70 showed that the accessibility of the anionic sulfhydryl reagent p-chloromercuribenzenesulfonate (pCMB

71 even low concentrations of the very specific sulfhydryl reagent p-chloromercuribenzoic acid (PCMB) in

72 The sulfhydryl reagent p-chloromercuriphenylsulfonate (1 mM)

73 Cys29 heme ligand toward modification by the sulfhydryl reagent p-mercuribenzoate, suggests that a co

74 In the absence of dithiothreitol and sulfhydryl reagents, PMIP27 yielded a mixture of monomer

75 es for alpha7-W55C nAChRs, whereas a neutral sulfhydryl reagent potentiated responses; residue C55 wa

76 Sulfhydryl reagents protected against modification of cy

77 ame resistant to p-CMPS, as predicted if the sulfhydryl reagent reacted with Cys80 in the wild-type e

78 -less CLH-3b mutant, we demonstrate that the sulfhydryl reagent reactivity of substituted cysteines a

79 harge restoration using a negatively charged sulfhydryl reagent reinstated also the WT phenotype.

80 S at pH 7.5, exhaustive reaction with either sulfhydryl reagent resulted in essentially 2 mol of cyst

81 Oxidation or labeling of hBCATm with sulfhydryl reagents results in enzyme inhibition.

82 However, both sulfhydryl reagents strongly inhibited the L750C mutant

83 A non-sulfhydryl reagent structurally related to NEM, N-ethyls

84 Both seHAS and spHAS were inhibited by sulfhydryl reagents such as N-ethylmaleimide (NEM) and i

85 ctobacillus casei TS inhibition studies with sulfhydryl reagents, the kinetics of inhibition suggeste

86 ine enhances the reaction of Cys-90 with the sulfhydryl reagents, thereby augmenting the increase in

87 Exposure to oxidative stress via the sulfhydryl reagent thimerosal resulted in a greater decr

88 was found to be insensitive to modulation by sulfhydryl reagents, this reactive sulfhydryl group is o

89 ed to the loss of the ability of the charged sulfhydryl reagents to inhibit NBMPR binding in isolated

90 However, the capacity of charged sulfhydryl reagents to inhibit the binding of NBMPR in b

91 ha7-W55C) and testing the ability of various sulfhydryl reagents to react with this cysteine.

92 1) exploit scanning cysteine mutagenesis and sulfhydryl reagents to show that the intracellular end o

93 th membrane-permeant and membrane-impermeant sulfhydryl reagents under a variety of conditions.

94 bition of transport by a membrane impermeant sulfhydryl reagent was diminished under conditions expec

95 endogenous cysteine to a membrane impermeant sulfhydryl reagent was enhanced by the D451E mutation, s

96 us cysteine residue to a membrane-impermeant sulfhydryl reagent was increased relative to wild type,

97 vity of the mutants to a membrane-impermeant sulfhydryl reagent was not conformationally sensitive.

98 ical modification of cysless E1371S/F508C by sulfhydryl reagents was used to probe the role of the si

99 nced rates of reaction of positively charged sulfhydryl reagents, we infer the presence of an electro

100 ys-C and labeling of cysteine residues using sulfhydryl reagents were consistent with a model where t

101 effects of both hydrophilic and hydrophobic sulfhydryl reagents were examined.

102 Six of these mutants reacted with charged sulfhydryl reagents, whereas bound antagonist only prote

103 d chloride leads to a reduced sensitivity to sulfhydryl reagents, whereas subsequent binding of GABA

104 r(607) did not respond to externally applied sulfhydryl reagent with significant changes in macroscop

105 e of hypoosmotic shock by reacting a charged sulfhydryl reagent with substituted cysteines.

106 Interactions of sulfhydryl reagents with introduced cysteines in the por