ライフサイエンスコーパス: 1-butanol

1 ty under high submicellar conditions (10-25% 1-butanol).

2 y and the inhibition of the Shaw2 channel by 1-butanol.

3 S4-S5 linkers conferred weak potentiation by 1-butanol.

4 ed by genistein, PD98059, and PLD-inhibitor, 1-butanol.

5 butane oxidation capability and accumulated 1-butanol.

6 inactivated was unable to grow on butane or 1-butanol.

7 y be more important in the detoxification of 1-butanol.

8 d the excess hydrogen-bond acceptor sites of 1-butanol.

9 well as leucine analogues, such as 3-methyl-1-butanol.

10 and elution with a 2:1 mixture of 1-propanol:1-butanol.

11 ediated signaling, 2,3-diphosphoglycerate or 1-butanol.

12 ethyl-2-buten-1-ol, and 300 mg/L of 3-methyl-1-butanol.

13 uction to 3-methyl-2-buten-1-ol and 3-methyl-1-butanol.

14 tectable 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol.

15 13)C,(1)H] correlations in the test molecule 1-butanol.

16 timulated ERK activity was also inhibited by 1-butanol.

17 However, they show increased resistance to 1-butanol.

18 atment of neutrophils with ethanol (0.8%) or 1-butanol (0.3%), which results in the accumulation of p

19 Application of 1-butanol (1-buOH), a selective inhibitor of PtdOH produ

20 ic compounds identified in this study, e.g., 1-butanol, 1-octen-3-ol, 2-and 3-methyl butanoic acid, h

21 Hexanal, 3-methyl-1-butanol, 1-pentanol, 1-octen-3-ol, acetic acid, furfur

22 s and higher alcohol esters, namely 3-methyl-1-butanol, 2,3-butanediol, ethyl lactate, 3-methyl-1-but

23 roduce higher alcohols including isobutanol, 1-butanol, 2-methyl-1-butanol, 3-methyl-1-butanol and 2-

24 of yeast promoted the formation of 3-methyl-1-butanol, 2-methyl-1-propanol and 3-(methylsulfanyl)-pr

25 d acetic acid, followed by hexanol, 3-methyl-1-butanol, 2-phenylethanol, 3-methylbutanal, hexanal, be

26 oline/1-octen-3-ol, for Venere, and 3-methyl-1-butanol/2-methyl-1-butanol, for Apollo, were also foun

27 ls including isobutanol, 1-butanol, 2-methyl-1-butanol, 3-methyl-1-butanol and 2-phenylethanol from g

28 aining emulsions had high levels of 2-methyl-1-butanol, 3-methyl-1-butanol, and 2-butanone after stor

29 sional spectra were acquired from samples of 1-butanol (55 nmol) and ethylbenzene (250 nmol).

30 ed urine 4-(methylnitrosamino)-1-(3-pyridyl)-1- butanol (a biomarker of cigarette smoke exposure) on

31 ry vesicles from the TGN was sensitive to 1% 1-butanol, a concentration that inhibited PLD-catalyzed

32 of BOH and BDH at three different levels of 1-butanol, a nontoxic level (0.1 mM), a growth-supportin

33 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanol, a validated tobacco-specific marker, was meas

34 presented the highest contents of 3/2-methyl-1-butanol, acetoin and organic acids.

35 known negative regulators of ABA signaling: 1-butanol, an inhibitor of phospholipase D, and abi1-1,

36 its activation by electron transfer to yield 1-butanol and (n-Bu3Sn)2O.

37 -azioctanol, the photoactivatable analogs of 1-butanol and 1-octanol, to photolabel the purified Ig1-

38 hol inhibition of WT-L1 adhesion was between 1-butanol and 1-pentanol.

39 PLD inhibitors 1-butanol and 2, 3-diphosphoglycerate, or the ARF6(N48R)

40 ethyl acetate, 2-methyl-1-propanol, 3-methyl-1-butanol and 2-methyl-1-butanol and furan derivatives l

41 ethyl acetate, 2-methyl-1-propanol, 3-methyl-1-butanol and 2-methyl-1-butanol was determined by means

42 nol, 1-butanol, 2-methyl-1-butanol, 3-methyl-1-butanol and 2-phenylethanol from glucose, a renewable

43 e exception of 2-methyl-1-propanol, 3-methyl-1-butanol and 2-phenylethyl alcohol, which decreased 68%

44 Inhibitors of phospholipase D (1-butanol and a dominant negative construct) prevented t

45 C4 column and were eluted with a mixture of 1-butanol and acetic acid.

46 d higher levels of 2-phenylethanol, 3-methyl-1-butanol and diethyl succinate, and lower concentration

47 1-propanol, 2-methyl-1-propanol, 3/2-methyl-1-butanol and ethyl octanoate were evaporated whereas th

48 -1-propanol, 3-methyl-1-butanol and 2-methyl-1-butanol and furan derivatives like 5-(hydroxymethyl)-2

49 on the inhibition of the K-Shaw2 channel by 1-butanol and halothane.

50 uptake; 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol and its glucuronides (total NNAL), a biomarker

51 well as 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol and its glucuronides (total NNAL), and cotinin

52 tions, we used a mixture of Triton X-100 and 1-butanol and observed that water-soluble natural and sy

53 y 56% and 44% conversions were achieved when 1-butanol and octadecanol were employed, respectively.

54 exanal concentration was higher and 2-methyl-1-butanol and toluene lower for C and GSC than for GSPC.

55 tes included n-pentane, n-hexane, n-heptane, 1 -butanol, and 1-pentanol.

56 he homologous series of 1-alkanols (ethanol, 1-butanol, and 1-hexanol) with Shaw2 K(+) channels in Xe

57 ation of four alcohols (ethanol, 1-propanol, 1-butanol, and 1-pentanol) to the corresponding carboxyl

58 high levels of 2-methyl-1-butanol, 3-methyl-1-butanol, and 2-butanone after storage.

59 ella, Lachnospiraceae, 4-methyl-2-pentanone, 1-butanol, and 2-butanone could discriminate NAFLD patie

60 effects for n-pentane, n-hexane, n-heptane, 1-butanol, and benzene solutes at infinite dilution.

61 aPKCs were inhibited by genistein, PD98059, 1-butanol, and expression of dominant-negative forms of

62 e, urine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol, and hair and nail nicotine levels were measur

63 enyl)-7H-pyrrolo[2,3-d]pyrimidin-4-y l]amino-1-butanol, and NBI-27914 at doses (30 mg/kg, i.p.) that

64 The substrate activation with ethanol and 1-butanol are explained by an ordered mechanism with an

65 that several biological processes blocked by 1-butanol are not affected by FIPI, suggesting the need

66 for oxidation of ethanol, cyclohexanol, and 1-butanol are quantitatively explained with the abortive

67 Commercial availability of (S)-2-methyl-1-butanol as a relatively inexpensive material suggested

68 Interestingly, replacing n-heptane with 1-butanol as a solvent led to a reactivity decrease of s

69 otope effect was determined to be 0.67 using 1-butanol as the substrate.

70 bly, rat NRK and GH3 cells were treated with 1-butanol, BFA, or nocodazole.

71 that increasing concentrations of ethanol or 1-butanol but not 2-butanol (0.05-0.5%) inhibited fMLP-i

72 e mutant of PLD1 or by the presence of 50 mM 1-butanol but not tert-butanol, an indication that these

73 O(2) and 5% CO(2)) in the presence of 0.05% 1-butanol, but not tertiary-butanol, stimulated PLD as e

74 Although production of 1-butanol by the fermentative coenzyme A (CoA)-dependent

75 ersion of the product of the PLD reaction by 1-butanol caused a partial loss of the [3H]thymidine res

76 were inhibited by genistein, PD98059, UO126, 1-butanol, cell-permeable myristoylated PKC-zeta pseudos

77 l, trans-2-hexenal) and alcohols (1-hexanol, 1-butanol, cis-3-hexenol) and had significant discrimina

78 During washout of 1-butanol, clathrin, a ubiquitous coat protein implicate

79 reover, the pretreatment of neutrophils with 1-butanol decreased Fgr activity in cells stimulated wit

80 Conversely, inhibition of PLD1 activity by 1-butanol decreases betaAPP trafficking in both wt and P

81 alkanols, the step that limits 2-butanol and 1-butanol dehydration rates; the latter two reactions sh

82 a grown on butane or 1-butanol expresses two 1-butanol dehydrogenases, a quinoprotein (BOH) and a qui

83 ol/vol) O(2), CuSO(4) (0.5 microM) repressed 1-butanol-dependent induction of beta-galactosidase acti

84 the mineral salts of standard growth medium, 1-butanol-dependent induction was significantly represse

85 kers showed that the potentiation induced by 1-butanol depends on the combination of a single mutatio

86 A structural analog of choline, 3,3-dimethyl-1-butanol (DMB), is shown to non-lethally inhibit TMA fo

87 However, 1-butanol does not always effectively reduce PA accumula

88 Inhibition of PLD activity by 0.1% 1-butanol during the initial 20 min of ABA treatment res

89 e solvent environment most closely resembles 1-butanol (epsilon = 17), although the energetic contrib

90 responses of Escherichia coli (DH5alpha) to 1-butanol exposure (1.2% [vol/vol]).

91 typic responses of E. coli to 1.2% (vol/vol) 1-butanol exposure included the following: (i) decreased

92 Pseudomonas butanovora grown on butane or 1-butanol expresses two 1-butanol dehydrogenases, a quin

93 1-Butanol extraction of chicken egg yolk homogenates con

94 y in organic solvents, ImmE1 was purified by 1-butanol extraction of isolated membranes, followed by

95 for Venere, and 3-methyl-1-butanol/2-methyl-1-butanol, for Apollo, were also found to act as ageing

96 time the direct photosynthetic production of 1-butanol from cyanobacteria Synechococcus elongatus PCC

97 bol-13-acetate-stimulated IL-8 production by 1-butanol further strengthened this observation.

98 1-Butanol had no effect on Cch-stimulated Pyk2, Ras, and

99 okers by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol had similar severity of lung injury as patient

100 nd urine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol identified 27 of the 28 nonsmokers by history

101 nd urine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol identified considerably more active smokers th

102 sing 100 mM sodium dodecyl sulfate (SDS) and 1-butanol in 10 mM sodium-phosphate (pH 7.2) at a flow r

103 opha H16, to produce isobutanol and 3-methyl-1-butanol in an electro-bioreactor using CO(2) as the so

104 from readily available aldehydes and 4-nitro-1-butanol in three steps.

105 Since 4-nitro-1-butanol in turn is prepared in two steps via Michael a

106 l compound using an alcohol (e.g., methanol, 1-butanol) in the presence of a relatively strong Lewis

107 1-Butanol increased Cch-stimulated protein secretion and

108 ications to the 2- and 3-carbon positions of 1-butanol increased potency, whereas modifications that

109 tion coefficients; e.g., the Kovats index of 1-butanol increases by more than 150 Kovats units.

110 le, brefeldin A (BFA), and primary alcohols (1-butanol) induce reversible fragmentation of the Golgi

111 alactosidase activity, was used to show that 1-butanol induced the BMO promoter in the presence or ab

112 Ethanol and 1-butanol inhibit L1-mediated cell-cell adhesion (L1 adh

113 1-Alcohols from methanol through 1-butanol inhibit with increasing potency the cell-cell

114 A screen for 1-butanol-insensitive mutants identified additional prot

115 butol [Emb; dextro-2,2'-(ethylenediimino)-di-1-butanol] is used to treat tuberculosis as well as diss

116 plets made of cetyltrimethylammonium bromide/1-butanol/isooctane.

117 tyrate and ethyl 2-methylbutyrate), 3-methyl-1-butanol, isopropyl acetate, and finally the two sulfid

118 on PKC translocation and degranulation, and 1-butanol itself had no effect on PKC translocation when

119 BOH exhibited high affinity towards 1-butanol (K(m) = 1.7 +/- 0.2 microM).

120 nts with 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol levels consistent with active smoking and was

121 nts with 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol levels in the active smoking range were younge

122 Urine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol levels were consistent with active smoking in

123 tectable 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol levels.

124 to the surface properties of neat water and 1-butanol liquids.

125 r under micellar conditions using 1-2% (v/v) 1-butanol mobile phase to remove plasma proteins and con

126 ributions suggests that the formation of the 1-butanol monolayer is driven by an excellent match betw

127 A dense 1-butanol monolayer is observed at the surface of the wa

128 g/L) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) (0.2 ng/L) along with the reduction of

129 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and its glucuronides (sum of which is d

130 smoking: 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and its O-glucuronide, 4-[(methylnitros

131 NNK) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) as the targets, we first developed a so

132 tabolite 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) in urine is frequently used as a biomar

133 rosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) is present in the urine of tobacco user

134 ine, and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), a metabolite of the powerful lung carc

135 abolite, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), is an important mechanism for 4-(methy

136 NK), and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), NNAL-N-beta-glucuronide, and NNAL-O-be

137 abolite, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), was sequestered in the lung.

138 product 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), which, in turn, can be glucuronidated,

139 urinary 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL).

140 omarker [4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL)], an established biomarker (cotinine),

141 tabolite 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol [NNAL]) and VOCs (including metabolites of the

142 The effects of ethanol and 1-butanol on cell-cell adhesion were antagonized by 1-pe

143 products due to the strong chemisorption of 1-butanol onto the Bronsted acid sites.

144 cal content of ImmE1 is approximately 80% in 1-butanol or 2,2,2-trifluoroethanol, consistent with a p

145 rgin whether PLD function was disrupted with 1-butanol or the small inhibitory RNAs.

146 NZVI (RL-Pd-NZVI) when reacted with TCE in a 1-butanol organic phase with limited amounts of water re

147 d BDH mRNAs were induced whenever the cell's 1-butanol oxidation activity was induced.

148 odel is proposed in which the electrons from 1-butanol oxidation follow a branched electron transport

149 ion of 1-hexanol production by extending the 1-butanol pathway provides the possibility to produce ot

150 holipase D (PLD) activity, the PLD inhibitor 1-butanol prevented the unsaturated fatty acid-induced r

151 ndent alcohol dehydrogenase (YqhD) increased 1-butanol production by 4-fold.

152 atio of the rates of 2-butanol production to 1-butanol production compared to Rev WT.

153 ation of Maillard reaction products 3-methyl-1-butanol, pyrazine, 2-ethylpyrazine, 2-ethyl-3-methylpy

154 us failed to reform efficiently after BFA or 1-butanol removal.

155 regulation of phosphoinositide production by 1-butanol resulted in diminished PIP(2) in the plasma me

156 D-mediated PA synthesis, by incubation with 1-butanol, resulted in the complete fragmentation of the

157 wth hormone and prolactin, were treated with 1-butanol resulting in the synthesis of phosphatidylbuta

158 h 0.4M perchloric acid and purification with 1-butanol significantly shortened sample preparation (30

159 iquid interfaces of mutually saturated water/1-butanol solutions at a temperature of 298.15 K were in

160 everal alcohols, notably isoamyl alcohol and 1-butanol, stimulate filamentous growth in haploid cells

161 by extending the coenzyme A (CoA)-dependent 1-butanol synthesis reaction sequence catalyzed by exoge

162 . butanovora could tolerate higher levels of 1-butanol than the P. butanovora boh::tet strain and the

163 Most significantly, in the presence of 1-butanol the architecture of the Golgi apparatus was di

164 en-1-ol, 3-methyl-2-buten-1-ol, and 3-methyl-1-butanol, three C5 alcohols that serve as potential bio

165 to Ala-33, increased the alcohol cutoff from 1-butanol to 1-decanol.

166 expressing wild-type Arf6 by treatment with 1-butanol to inhibit the formation of phosphatidic acid

167 ce of nucleophilic and biomimetic substrates 1-butanol, tosylhydrazine, or tetrahydrofurfuryl alcohol

168 nalytical methodologies were applied to both 1-butanol-treated and control cells to draw correlations

169 -1-propanol, 3-methyl-1-butanol and 2-methyl-1-butanol was determined by means of head space solid ph

170 story or 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol was not associated with acute respiratory dist

171 by urine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol was significantly associated with acute respir

172 3-Methyl-1-butanol was the major compound identified in the ferme

173 Instead, upon 1-butanol washout, it maintained a compact, tight morpho

174 tanoate, whereas phenyl ethanol and 3-methyl-1-butanol were dominating alcohols.

175 the TSNA 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol were identified and quantified in authentic dr

176 anone, 2-pentanone, 2-heptanone and 3-methyl-1-butanol were identified as relevant VOCs for Lactobaci

177 anone, 2-pentanone, 2-heptanone and 3-methyl-1-butanol were identified as relevant VOCs for Lactobaci

178 2-Butanone and 3-methyl-1-butanol were identified in Lactococcus lactis subsp. l

179 2-Butanone and 3-methyl-1-butanol were identified in Lactococcus lactis subsp. l

180 Beas-2B exposure to 1-butanol, which converts the PLD-generated phosphatidic

181 Incubating embryos with 1-butanol, which diverts production of phosphatidic acid

182 on of PA is inhibited by the primary alcohol 1-butanol, which has thus been widely employed to identi

183 broblasts deficient in PLD activity and also 1-butanol, which inhibits phosphatidic acid production b

184 resistant membrane fractions is inhibited by 1-butanol, which subverts production of phosphatidic aci

185 sporulation, because treatment of cells with 1-butanol, which supports Spo14p-catalyzed PtdCho breakd

186 edium in the presence of different levels of 1-butanol, wild-type P. butanovora could tolerate higher

187 An abrupt cutoff exists after 1-butanol, with 1-pentanol and higher 1-alcohols showing

188 ten from flour defatted with water-saturated 1-butanol (WSB; extracted at 20 degrees C) and 2-propano

189 ith adenoviruses overnight or the inhibitors 1-butanol, Y-27632, or C3 exotoxin before stimulation wi