ライフサイエンスコーパス: aminoethyl

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1 ethylammonium/Cholesterol/DSPE-PEG-anisamide aminoethyl.

2 -monooxygenase (DbetaM; E.C. 1.14.17.1)/1-(2-aminoethyl)-1,4-cyclohexadiene (CHDEA) reaction partitio

3 Easily accessible 2-(2-aminoethyl)-1-aryl-3,4-dihydropyrazino[1,2-b]indazole-2-

4 with the NO donor 1-hydroxy-2-oxo-3,3-bis(3-aminoethyl)-1-triazene (300 microM) caused a decrease in

5 1,3-bis(aminomethyl)phenyl group with a 5-(2-aminoethyl)- (18) or a 5-(2-dimethylaminoethyl)- substit

6 l substituent as a precursor of the key 5-(2-aminoethyl)-1H-quinolin-4-one intermediate.

7 sulfhydryl-specific iron complex of EDTA-2- aminoethyl 2-pyridyl disulfide (EPD-Fe).

8 were modified with an iron complex of EDTA-2-aminoethyl 2-pyridyl disulfide.

9 containing 2'-O-methoxy (2'-OMe) and 2'-O-(2-aminoethyl) (2'-AE) ribose substitutions in varying prop

10 len-linked TFOs with 2'-O-methyl and 2'-O-(2-aminoethyl) (2'-AE) substitutions that are active in a g

11 3-(trifluoromethyl)-diazirin-3-yl]benzoyl-(2-aminoethyl) ]-2 '-deoxyadenosine-5'-triphosphate (DB-dAT

12 '-deoxyadenosine-5'-monophosphate to N(6)-(2-aminoethyl)-2'-deoxyadenosine-5'-monophosphate (N(6)-dAM

13 and continues with rearrangement of N(1)-(2-aminoethyl)-2'-deoxyadenosine-5'-monophosphate to N(6)-(

14 the material is deprotected to yield N(6)-(2-aminoethyl)-2'-deoxyadenosine-5'-triphosphate (N(6)-dATP

15 active dATP analogs, N(6)-[4-azidobenzoyl-(2-aminoethyl)]-2'-deoxyadenosine-5'-triphospha+ ++ te (AB-

16 betaV229C also reacted with 2-aminoethyl-2-aminoethanethiosulfonate (AEAETS) and with

17 least two of these compounds, 7-(1-hydroxy-2-aminoethyl)-3,4-dihydro-5- hydroxy-2H-1,4-benzothiazine-

18 ine-3-carboxylic acid (9) and 8-(1-hydroxy-2-aminoethyl)-3,4-dihydro-5-hydroxy-2H-1, 4-benzothiazine-

19 y 3-aminopropyltriethoxysilane (APTES), N-(2-aminoethyl)-3-aminopropyltriethoxysilane (AE-APTES) and

20 N-(2-Aminoethyl)-3-aminopropyltrimethoxysilane (AATM, NH2(CH2

21 on of the resulting HOOC-Phe-SWCNT with 1-(3-aminoethyl)-4,4'-bipyridinium bromine and N-alkylation w

22 One such compound, N-(2-aminoethyl)-5-chloroisoquinoline-8-sulfonamide (CK17), i

23 the casein kinase I-specific inhibitor, N-(2-aminoethyl)-5-chloroisoquinoline-8-sulfonamide (CKI-7);

24 Thus, 4-(2-aminoethyl)-6,7-dimethoxy-2,3-dihydrobenzofuran hydrochl

25 has been developed to functionalize the 4-(2-aminoethyl)-6-dibenzofuran propionic acid residue (1a) a

26 ha-amino acid-based beta-turn mimetic (4-(2'-aminoethyl)-6-dibenzofuran propionic acid residue, 1), w

27 5'-S-(2-aminoethyl)-6-N-(4-nitrobenzyl)-5'-thioadenosine (SAENTA

28 via the 7-deazaguanosine precursor preQ1 (7-aminoethyl 7-deazaguanine) by an uncharacterized pathway

29 ctive alkylation of indoles with N-protected aminoethyl acetals in the presence of TES/TFA is reporte

30 Recently, pyrimidine TFOs with 2'-O-aminoethyl (AE) substitutions were shown to have enhance

31 intermediate in the [5 + 5] synthesis of an aminoethyl aglycon-equipped decasaccharide, correspondin

32 noyl)-L-3-(tert-bu tyl)-alanyl-l -alanine, 2-aminoethyl amide), which has previously been shown to in

33 entano)-L-3-(tert-butyl)-alanyl-L-alanine, 2-aminoethyl amide, which blocks leukocyte TNF, TNF recept

34 pper(II) bromide and Me6-TREN (TREN = tris(2-aminoethyl amine)), semi-fluorinated monomers with side

35 Sulfonamide and amide derivatives of tris(aminoethyl)amine (TREN) are known to facilitate phosphol

36 inonate (1,2-HOPO) binding units on a tris(2-aminoethyl)amine (tren) backbone, [tren(CAM)(m)(1,2-HOPO

37 p-tert-butylbenzoic (for 9) acid with tris(2-aminoethyl)amine (tren) were used together with tetraben

38 ing selectivities and reactivity with tris(2-aminoethyl)amine (tren), which enabled the design of a m

39 e presence of a triamide derived from tris(2-aminoethyl)amine (tren), which is known to function as a

40 We have identified tris(2-aminoethyl)amine (tren)-derived scaffolds with two (t2M)

41 pyr and N,N',N''-tris(2-pyridylmethyl)tris(2-aminoethyl)amine (trenpyr).

42 lene frame with tripodal units (e.g., tris(2-aminoethyl)amine [tren]) through postsynthetic modificat

43 ffold, TREN-(suc-OH)(3) where TREN is tris(2-aminoethyl)amine and suc is the succinic acid spacers, w

44 at amide and sulfonamide derivatives of tris(aminoethyl)amine facilitate phospholipid flip-flop acros

45 wo core units; 1,7-diaminoheptane and tris(2-aminoethyl)amine have been used to produce the final den

46 rtiary amine ligand (Me6-Tren; Tren = tris(2-aminoethyl)amine), near-quantitative monomer conversion

47 One of the receptors consists of two tris(2-aminoethyl)amine-derived binding subunits separated by p

48 scence donor/quencher system, in which 5-[(2-aminoethyl) amino]naphthalene-1-sulfonic acid (EDANS) an

49 an adduct of GTPgammaS and (5-(2(iodoacetyl)aminoethyl)amino)naphthalene-1-sulfonic acid (dnsGTP), a

50 BMS-345541 (4(2'-aminoethyl)amino-1,8-dimethylimidazo(1,2-a)quinoxaline)

51 ted by the selective IKKbeta inhibitor 4-(2'-aminoethyl)amino-1,8-dimethylimidazo[1,2-a]quinoxaline (

52 rimidinediyl)bis(methylene)]phenol and 8-[(2-aminoethyl)amino]-3,7-dihydro-3-methyl-7-(3-phenoxypropy

53 A functionalized congener bearing an [(aminoethyl)amino]carbonyl group was also prepared as an

54 t, 7-[[(2-(3-(125I-p-hydroxyphenyl)propionyl)aminoethyl)amino]carbonyl]-7-+ ++desacetyl-forskolin([12

55 wo new fluorogenic substrates, Arg-Glu(5-[(2-aminoethyl)amino]naphthalene-1-sulfonic acid (EDANS))-Gl

56 enicillamine or (Z)-1-[N-(2-aminoethyl)-N-(2-aminoethyl)-amino]-diazen-1-ium-1,2-diolate inhibited RA

57 lpenicillamine, (Z)-1-[N-(2-aminoethyl)-N-(2-aminoethyl)-amino]-diazen-1-ium-1,2-diolate, and a nitro

58 xamidoad eno sine (15 nM) and [3H]8-[4-[[[[2-aminoethyl)-amino]carbonyl]methyl]oxy]phenyl]-1,3- dipro

59 ZnAF-2 {6-[N-[N',N'-bis(2-pyridinylmethyl)-2-aminoethyl]amino-3',6'-dihydroxyspir o[isobenzofuran-1(3

60 on was facilitated using a solid phase, N-(2-aminoethyl)aminomethyl polystyrene.

61 among these compounds is (4S)-N-(4-amino-5-[aminoethyl]aminopentyl)-N'-nitroguanidine (7) (K(i) = 12

62 cked by the nNOS inhibitor (4S)-N-(4-amino-5[aminoethyl]aminopentyl)-N'-nitroguanidine and the calmod

63 ck nitric oxide synthesis; (4S)-N-(4-Amino-5[aminoethyl]aminopentyl)-N'-nitroguanidine, TFA, a neuron

64 ME at a high dose, but not (4S)-N-(4-Amino-5[aminoethyl]aminopentyl)-N'-nitroguanidine, TFA, decrease

65 e synthase inhibitor AAAN (N-(4S)-4-amino-5-[aminoethyl]aminopentyl-N'-nitroguanidine; 10 mumol l(-1)

66 d of N,N-distearyl-N-methyl-N-2-(N'-arginyl) aminoethyl ammonium chloride (DSAA), a guanidinium-conta

67 i.e. N,N-distearyl-N-methyl-N-2-(N'-arginyl) aminoethyl ammonium chloride, which can induce reactive

68 r 8 and 9 and leads to the formation of N-(2-aminoethyl)- and N-(2-hydroxyethyl)-N-nitrosoformamides

69 rase-II (CA-II) analyte and immobilized 4-(2-aminoethyl)benzenesulfonamide (ABS) ligand display a 100

70 ves of 2 carbonic anhydrase inhibitors, 4-(2-aminoethyl)benzenesulfonamide (AEBS) and 4-aminobenzensu

71 plasma, was completely inhibited by 0.2 mM p-aminoethyl benzenesulfonyl fluoride (Pefabloc), a new se

72 eoblastic lineage cells, was blocked by 4-(2-aminoethyl) benzenesulfonyl fluoride hydrochloride (AEBS

73 hibited by 1400W, an iNOS inhibitor, by 4-(2-aminoethyl) benzenesulfonyl fluoride, an inhibitor of NA

74 t effectively inhibited by antipain and 4-(2-aminoethyl) benzenesulfonyl fluoride, was metal ion-depe

75 DPH oxidase blockers acetovanillone and 4-(2-aminoethyl)benzenesulfonyl fluoride (AEBSF), whereas the

76 of CM with serine proteinase inhibitors 4-(2-aminoethyl)benzenesulfonyl fluoride and diisopropyl fluo

77 red with the serine protease inhibitor, 4-(2-aminoethyl)benzenesulfonyl fluoride hydrochloride (AEBSF

78 includes the serine-protease inhibitor 4-(2-Aminoethyl)benzenesulfonyl fluoride hydrochloride (AEBSF

79 bition of serine protease activity with 4-(2-aminoethyl)benzenesulfonyl fluoride hydrochloride (AEBSF

80 blocked with serine protease inhibitor 4-(2-aminoethyl)benzenesulfonyl fluoride hydrochloride, 64-88

81 are blocked by mineralization inhibitor 4-(2-aminoethyl)benzenesulfonyl fluoride hydrochloride.

82 ically by the serine protease inhibitor 4-(2-aminoethyl)-benzenesulfonyl fluoride (AEBSF), but not by

83 ell-permeant serine protease inhibitors 4-(2-aminoethyl)-benzenesulfonyl fluoride and N(alpha)-p-tosy

84 The serine protease inhibitor 4-(2-Aminoethyl)-benzenesulfonyl fluoride blocked the effects

85 sitive to the serine protease inhibitor 4-(2-aminoethyl)-benzenesulfonyl fluoride hydrochloride (AEBS

86 cin and 2-deoxyglucose was inhibited by 4-(2-aminoethyl)-benzenesulfonyl fluoride hydrochloride, a se

87 4-(2-Aminoethyl)-benzenesulfonyl fluoride, a specific inhibit

88 f heme ligands such as oxygen, cyanide, 4-(2-aminoethyl)-benzenesulfonyl fluoride, and CO.

89 ibitors, diphenyleneiodonium (DPI), and 4-(2-aminoethyl)-benzenesulfonyl fluoride, but not with the n

90 itors phenylmethylsulfonyl fluoride and 4-(2-aminoethyl)-benzenesulfonyl fluoride.

91 ively, of the protease inhibitor AEBSF [4-(2-aminoethyl)-benzenesulfonyl fluoride].

92 or specific serine protease inhibitors 4-(2-Aminoethyl)benzenesulfonylfluoride and diisopropylfluoro

93 ere screened, serine protease inhibitor 4-(2-aminoethyl)benzenesulfonylfluoride HCl (AEBSF) was the o

94 functionalized graphite electrode with 4-(2-aminoethyl) benzoic acid.

95 roscopy tips carrying either thioglucose, 2'-aminoethyl beta-d-glucopyranoside, or aminophlorizin.

96 by using the small intracellular tracer N-(2-aminoethyl) biotinamide hydrochloride.

97 cells readily passed Lucifer yellow and N-(2-aminoethyl)biotinamide hydrochloride (neurobiotin); in c

98 have been synthesized, based on 2'(3')-O-(2-aminoethyl)carbamoyl-ATP (edaATP).

99 hylanthraniloyl) GTP (mantGTP), 2'(3')-O-[(2-aminoethyl)carbamyl] GTP (edGTP), and adducts of fluores

100 ignaling with R-(+)-trans-N-(4-pyridyl)-4-(1-aminoethyl)-cyclohexane carboxamide (Y27632) can markedl

101 o-kinase (ROCK) inhibitor N-(4-pyridyl)-4-(1-aminoethyl)cyclohexanecarboxamide dihydrochloride (Y2763

102 ) and Rho kinase [Y27632 (N-(4-pyridyl)-4-(1-aminoethyl)cyclohexanecarboxamide dihydrochloride)]} but

103 e inhibitor (R)-(+)-trans-N-(4-pyridyl)-4-(1-aminoethyl)-cyclohexanecarboxamide, 2 HCl (Y-27632) had

104 or Y27632 [(R)-(+)-trans-N-(4-pyridyl)-4-(1-aminoethyl)-cyclohexanecarboxamide], both NSAID drugs st

105 or, Y27632 [(R)-(+)-trans-N-(4-pyridyl)-4-(1-aminoethyl)-cyclohexanecarboxamide].

106 from vaccinia virus) was modified to S-(beta-aminoethyl)cysteine (gamma-thialysine) using freshly pre

107 eoxycytidine analog, 4-[N-(p-azidobenzoyl)-2-aminoethyl]-dCTP (ABdCTP), has been synthesized and inco

108 ytrityl-3'-O-tert-butyldimethylsilyl-N(4)-(2-aminoethyl)deoxycy tidine to give the cross-link.

109 indoles was prepared and several substituted aminoethyl derivatives were active (23-27, 5) at the CB(

110 gonists xestospongin-C (Xe-C; 2 microM) or 2-aminoethyl diphenylborate (2-APB; 25 microM), and by rya

111 The presence of 2-aminoethyl diphenylborate differentially affected the re

112 BL-2H3 cells with LY294002 or Deltap85 and 2-aminoethyl diphenylborate, a cell-permeant antagonist of

113 One potent activator of TRPV3 is 2-aminoethyl diphenylborinate (2-APB), a synthetic chemica

114 reversed by the Ca(2+) channel inhibitors 2-aminoethyl diphenylborinate and SKF-96365.

115 2-Aminoethyl diphenylborinate but not SKF-96365 abrogated

116 2-Aminoethyl diphenylborinate was recently identified as a

117 ydrochloride), flufenamic acid, and 2-APB (2-aminoethyl diphenylborinate) potently inhibited the lept

118 eceptor potential) channel blockers 2-APB (2-aminoethyl diphenylborinate), flufenamic acid, SKF96365

119 henylaminoethyl-, and o-nitrophenyl-N-methyl-aminoethyl-diphosphate.beryllium fluoride have been dete

120 e was performed using diphenylborinic acid 2-aminoethyl ester (DPBA) as inducer of regioselectivity.

121 The Ca2+ chelator, ethylene glycol-bis (beta-aminoethyl ether) N',N',N', N'-tetraacetic acid (EGTA),

122 the enzyme, while ethylene glycol-bis (beta-aminoethyl ether) N,N,N',N'-tetraacetic acid (EGTA) and

123 tracellular Ca2+ or ethyleneglycol-bis (beta-aminoethyl ether)- N,N,N',N' -tetraacetic acid to reduce

124 uoperazine, W7, or ethylene glycol-bis-(beta-aminoethyl ether)-N,N'-tetraacetic acid (EGTA) + calcium

125 with the calcium chelator ethyleneglycol-bis(aminoethyl ether)-N,N'-tetraacetic acid, suggesting that

126 ain in a Gd3+, La3+, ethyleneglycol-bis(beta-aminoethyl ether)-N,N'-tetraacetic acid-, and RR-sensiti

127 netetraacetate and by ethyleneglycolbis(beta-aminoethyl ether)-N,N'-tetraacetic acid.

128 ls during removal with ethylene glycol bis(2-aminoethyl ether)-N,N,N',N'- tetraacetic acid.

129 Gadolinium, ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) + 1,

130 ting agents such as ethylene glycol bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) coul

131 d calcium chelator ethylene glycol-bis (beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) in t

132 er containing 1 mM ethylene glycol bis-(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA), glu

133 Ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA)-trea

134 hermore, addition of ethyleneglycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid completely

135 tion of the chelator ethyleneglycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid to migratio

136 llular calcium with ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid-acetoxy-met

137 high-intracellular ethylene glycol-bis(alpha-aminoethyl ether)-N,N,N'N'-tetraacetic acid (20 mM).

138 effect of calcium, ethyleneglycol-bis-(beta-aminoethyl ether)-N-N' -tetraacetic acid (EGTA) and calc

139 ium containing 5 mM ethylene glycol-bis[beta-aminoethyl ether]N,N'-tetraacetic acid (EGTA) and no del

140 D ODN with thermolytic 2-(N-formyl-N-methyl)aminoethyl (fma) phosphate/thiophosphate protecting grou

141 in conjugating activity of crude and diethyl aminoethyl-fractionated liver cytosols of ethanol-fed ra

142 which the nucleobases are linked by an N-(2-aminoethyl) glycine backbone.

143 dification at the gamma-position of the N-(2-aminoethyl) glycine unit can transform a randomly folded

144 phate backbone has been replaced by the N-(2-aminoethyl) glycine units.

145 omising precursor to RNA, consisting of N-(2-aminoethyl)glycine (AEG) and the adenine, uracil, guanin

146 e discovered that cyanobacteria produce N-(2-aminoethyl)glycine (AEG), a backbone for peptide nucleic

147 rick base pairing rules, but contains a N-(2-aminoethyl)glycine backbone in place of the deoxyribose

148 a- instead of the alpha-position of the N-(2-aminoethyl)glycine backbone unit.

149 monoclonal HNK-1 antibodies from rodents: 2-aminoethyl glycosides of selectively O-sulfated trisacch

150 d several structural elements, including the aminoethyl group (VMAT recognition), halogenated hydroxy

151 pening followed by hydrolytic removal of the aminoethyl group from the quinone ring.

152 support-bound oligomer was displaced by the aminoethyl group of 5'-dimethoxytrityl-3'-O-tert-butyldi

153 -1-phenylethyl and 2-[N-methyl-N-(2-pyridyl)]aminoethyl groups are particularly promising for 5'-hydr

154 H 7.0, cleavage of 2-[N-methyl-N-(2-pyridyl)]aminoethyl groups occurs spontaneously when their phosph

155 ed to tag the phosphate backbone of DNA with aminoethyl groups.

156 9-[N-(2-carboxyethyl)-N-(2-phosphonoethyl)-2-aminoethyl]guanine has a K(i) of 50 nM, the best inhibit

157 er containing N1-methylhypoxanthine or N1-(2-aminoethyl)-hypoxanthine has a reduced thermostability w

158 ypoxanthine, N1-methylhypoxanthine and N1-(2-aminoethyl)-hypoxanthine.

159 -methoxy-3-oxopropyl)-N-(2-phosphonoethyl)-2-aminoethyl]hypoxanthine (K(i) = 100 nM): no inhibition c

160 ng a pharmacophoric model of binding of 3-(2-aminoethyl)indoles to 5HT(1B/1D) receptors, we identifie

161 e most potent AChE inhibitors were 120 (3-(2-aminoethyl) indolin-4-yl ethyl(methyl)carbamate dihydroc

162 The reactivity of N-Boc-protected 2-benzyl-2-aminoethyl iodide was found to be superior to the less s

163 ive inhibitor of inducible NO synthase (S-(2-aminoethyl)-isothiourea) or a NO scavenger ([2-(4-carbox

164 rves as a target for the antimetabolite S-(2-aminoethyl)-L-cysteine (AEC).

165 , the K(i) values for aminoacylation of S-(2-aminoethyl)-l-cysteine and l-lysinamide were over 180-fo

166 h inhibition imparted by LysRS1 against S-(2-aminoethyl)-l-cysteine and LysRS2 against gamma-aminobut

167 highly effective discrimination against S-(2-aminoethyl)-L-cysteine by class I LysRS and correlates w

168 y allowed up to a 4-fold improvement in S-(2-aminoethyl)-L-cysteine discrimination.

169 f several hundred-fold in efficiency of S-(2-aminoethyl)-L-cysteine utilization, this was uniformly a

170 etermined for the nonprotein amino acid S-(2-aminoethyl)-L-cysteine, a potent inhibitor of LysRS2.

171 Cystathionine and S-aminoethyl-L-cysteine were also substrates for the prote

172 (from cystathionine), and cysteamine (from S-aminoethyl-L-cysteine).

173 ontaining the inhibitory lysine analogue S-2-aminoethyl-L-cysteine.

174 dyl 4-18F-fluorobenzoate (18F-SFB) with N-(2-aminoethyl)maleimide.

175 s pyrene-maleimidyl-S-CoA and BODIPY-FL-N-(2-aminoethyl)maleimidyl-S-CoA were enzymatically loaded on

176 dom copolymer rich in primary amines, poly(2-aminoethyl methacrylate hydrochloride-co-2-hydroxyethyl

177 acrylic acid N-hydroxysuccinimide ester or 2-aminoethyl methacrylate into OEGMA-based polymers.

178 ationary phases prepared with the N-methyl-2-aminoethyl methacrylate platform exhibit the best select

179 olymer hybrid of P22 and cross-linked poly(2-aminoethyl methacrylate) could be useful as a new high-d

180 ine mutants were also most susceptible to (2-aminoethyl)-methane thiosulfonate and N-ethylmaleimide m

181 ge, and susceptibility to modification by (2-aminoethyl)-methane thiosulfonate and N-ethylmaleimide o

182 N-Ethylmaleimide, (2-aminoethyl)-methane thiosulfonate, 2-aminoethoxydiphneyl

183 rious times with a rapid blocking reagent, 2-aminoethyl methanethiosulfonate (AEMTS), fractionating t

184 he substituted cysteine to modification by 2-aminoethyl methanethiosulfonate (MTS-EA) in excised macr

185 2-Aminoethyl methanethiosulfonate (MTSEA(+)) failed to mod

186 e to inhibition by the sulfhydryl reagents 2-aminoethyl methanethiosulfonate (MTSEA) and 2-(trimethyl

187 Parachloromercuribenzoic acid and 2-aminoethyl methanethiosulfonate (MTSEA), which share wit

188 as then measured in the presence of 2.5 mM 2-aminoethyl methanethiosulfonate hydrobromide (MTSEA) or

189 residues (substituted for D43 and T47) by 2-aminoethyl methanethiosulfonate in the GABAA alpha1 subu

190 outer third of alphaM1, which reacted with 2-aminoethyl methanethiosulfonate only in the presence of

191 enched at various times by the addition of 2-aminoethyl methanethiosulfonate to block unreacted sulfh

192 all, sulfhydryl-specific, charged reagent, 2-aminoethyl methanethiosulfonate with cysteines substitut

193 reated with the primary amine reagent MTSEA (aminoethyl methanethiosulfonate) retain alpha-btx bindin

194 Sulfhydryl modification of Y124C by 2-aminoethyl methanethiosulfonate, but not by N-ethylmalei

195 -disulfide intermediates were blocked with 2-aminoethyl methanethiosulfonate, fractionated using ion-

196 l methanethiosulfonate, positively charged 2-aminoethyl methanethiosulfonate, or 2-trimethylammonioet

197 extracellularly and intracellularly added 2-aminoethyl methanethiosulfonate, we previously located t

198 pulldown assays with membrane-impermeable 2-aminoethyl methanethiosulfonate-biotin and streptavidin

199 D2 and the TMD2-3 loop domain reacted with 2-aminoethyl methanethiosulfonate-biotin, establishing aqu

200 protected by quinacrine from reaction with 2-aminoethyl methanethiosulfonate.

201 sensitive to the polar sulfhydryl reagent 2-aminoethyl methanethiosulfonate.

202 er of the two cysteines to modification by 2-aminoethyl methanethiosulfonate.

203 In contrast, the smaller compound, 2-(aminoethyl) methanethiosulfonate (MTSEA), modified a pos

204 m)ethyl]methanethiosulfonate (MTSET), and (2-aminoethyl) methanethiosulfonate (MTSEA).

205 Pretreatment with (2-aminoethyl)methanethiosulfonate (MTSEA) inhibited [(3)H]

206 By contrast, bath application of (2-aminoethyl)methanethiosulfonate (MTSEA) to closed channe

207 yramine increased the rate of reaction of (2-aminoethyl)methanethiosulfonate (MTSEA) with X-A342C, th

208 at position 172, which reacted with both (2-aminoethyl)methanethiosulfonate and N-biotinylaminoethyl

209 ls were gating were also modified by 1 mm (2-aminoethyl)methanethiosulfonate applied in the absence o

210 eactive methanethiosulfonate derivatives ((2-aminoethyl)methanethiosulfonate hydrobromide (MTSEA) and

211 2-(Aminoethyl)methanethiosulfonate hydrobromide (MTSEA) fai

212 ne analog binding by the cysteine reagent 2-(aminoethyl)methanethiosulfonate hydrobromide (MTSEA) in

213 is subsequently covalently modified with (2-aminoethyl)methanethiosulfonate hydrobromide, a reagent

214 d Res-FLAG, the amount of inactivation by (2-aminoethyl)methanethiosulfonate was less than expected i

215 nctionally sensitive to the inhibition by (2-aminoethyl)methanethiosulfonate.

216 susceptibility to polar MTS derivatives [(2-aminoethyl)-methanethiosulfonate (MTSEA), [2-(trimethyla

217 ere accessible to both outside and inside 2-(aminoethyl)-methanethiosulfonate hydrobromide (MTSEA) Fu

218 2-(Aminoethyl)-methanethiosulfonate hydrobromide (MTSEA)-bi

219 Cys43 and Cys47 were accessible to 2-aminoethyl methanethiosulphonate (MTSEA) modification, w

220 3C or T47C substitutions were sensitive to 2-aminoethyl methanethiosulphonate (MTSEA) modification.

221 ChR subunits, we used the sulphydryl agent 2-aminoethyl methanethiosulphonate (MTSEA), which has prev

222 or His, or Cys followed by treatment with 2-aminoethyl methanethiosulphonate) greatly enhanced outwa

223 ing agents such as iodoacetamide (IA) and (2-aminoethyl)methanethiosulphonate (MTSEA) also bind and a

224 t with the methanethiosulphonate compound (2-aminoethyl)methanethiosulphonate (MTSEA, 2.5 mM), but we

225 2-Aminoethyl methylphosphonate (2-AEMP), an analog of GABA

226 sulfonate (MTSES), or the positively charged aminoethyl methylthiosulfonate (MTSEA), has little or no

227 roup (i.e., ester 26), or cyclization of the aminoethyl moiety to a carbazole (e.g., 34, 36) or beta-

228 inoline core, appended with a required basic aminoethyl moiety, and with potency- and property-modula

229 nvestigate the optimal conformation of the 2-aminoethyl moiety.

230 er scanning microscopy (CLSM) as well as a 2-aminoethyl-monoamide-DOTA group for loading stable europ

231 Inclusion of positively charged 2-aminoethyl-MTS (MTSEA) within the electrode solution red

232 cetylpenicillamine and spermine NONOate [N-(-aminoethyl)N-(2-hydroxy-2-nitrohydrazino)-1,2-ethylenedi

233 stores release, and ethyleneglycol-bis-(beta-aminoethyl)- N,N,N',N'-tetra-acetic acid (EGTA) suppress

234 S-nitroso-N-acetylpenicillamine, (Z)-1-[N-(2-aminoethyl)-N-(2-aminoethyl)-amino]-diazen-1-ium-1,2-dio

235 nitroso-N-acetylpenicillamine or (Z)-1-[N-(2-aminoethyl)-N-(2-aminoethyl)-amino]-diazen-1-ium-1,2-dio

236 ) with nitric oxide donors (e.g. (Z)-1-[2-(2-aminoethyl)-N-(2-ammonio-ethyl)amino]diazen-1-ium-1, 2-d

237 hMSC) with a nitric oxide donor, (Z)-1-[N-(2-aminoethyl)-N-(2-ammonioethyl) aminio] diazen-1-ium-1,2-

238 tration of a nitric oxide donor, (Z)-1-[N-(2-aminoethyl)-N-(2-ammonioethyl) aminio]diazen-1-ium-1,2-d

239 rtic endothelial cells (BAEC) to (Z)-1-[N-(2-aminoethyl)-N-(2-ammonioethyl) amino]diazen-1-ium-1,2-di

240 ment of cells with the NO donors (Z)-1-[2-(2-aminoethyl)-N-(2-ammonioethyl) aminodiazen-1-ium-1,2-dio

241 e reaction could be inhibited by (z)-1-[2-(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1- ium-1, but

242 etyl-D,L-penicillamine [SNAP] or (Z)-1-[2-(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1- ium-1,2-di

243 Moreover, NO precursor (Z)-1-[2-(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-dio

244 n for 12 hours with 150 micromol/L (Z)-1-[(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-dio

245 mino-l-arginine) or a (.)NO donor ((Z)-1-[(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-dio

246 ion of E. coli with the NO donor (Z)-1-[N-(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-dio

247 with the nitric oxide (NO) donor, (z)-1-2-[2-Aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-dio

248 with an NO. donor, DETANONOATE ((Z)-1-[2-(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-dio

249 ed in the presence of TRPM8 antagonist, N-(2-aminoethyl)-N-(4-(benzyloxy)-3-methoxybenzyl)thiophene-2

250 We studied N-(2-aminoethyl)-N-(4-(benzyloxy)-3-methoxybenzyl)thiophene-2

251 d from 2,6-diformyl-4-methylphenol and bis(2-aminoethyl)-N-methylamine) are described.

252 M) analogues have been synthesized: N5-[4-(2-aminoethyl-o-carboranyl)butyl] and N5- inverted question

253 rosine) and pulcherosine (5-[4"-(2-carboxy-2-aminoethyl)phenoxy]3, 3'-dityrosine) by high resolution

254 identified isodityrosine (3-[4'-(2-carboxy-2-aminoethyl)phenoxy]tyrosine), a non-fluorescent product

255 g these compounds is N-(4S)-[4-amino-5-[2-(2-aminoethyl)phenylamino]-pentyl]-N'-nitroguanidine (17) (

256 21680 (4-((N-ethyl-5'-carbamoyladenos-2-yl)-aminoethyl)-phenylpropionic acid) had no effect.

257 te ligands, N-(4'-trifluoromethoxybenzoyl)-2-aminoethyl phosphate (F6) and N-(4'-trifluoromethoxybenz

258 and N-(4'-trifluoromethoxybenzenesulfonyl)-2-aminoethyl phosphate (F9), that were previously shown to

259 ncludes aminomethyl phosphonate [AMP](2-), 1-aminoethyl phosphonate [1AEP](2-), 2-aminoethyl phosphon

260 (2-), 1-aminoethyl phosphonate [1AEP](2-), 2-aminoethyl phosphonate [2AEP](2-), aminopropyl phosphona

261 alcohol has allowed us to introduce cationic aminoethyl phosphotriester modifications into ODNs.

262 micked by the H1 receptor agonist alpha-2-(2-aminoethyl)pyridine (AEP).

263 ort the discovery of chiral acetyl-protected aminoethyl quinoline ligands that enable asymmetric pall

264 (pdU), 2'-O-methyl-ribose (2'-O-Me), 2'-O-(2-aminoethyl)-ribose, or 2'-O, 4'-C-methylene bridged or l

265 sing a structural analogue, 4-fluorophenyl 2-aminoethyl selenide (FPAESe) as an internal standard.

266 elenium compound, 4-hydroxyphenyl 2-methyl-2-aminoethyl selenide (HOMePAESe), were unsuccessful becau

267 e 4B affinity chromatography, and quaternary aminoethyl-Sephadex column chromatography, and the seque

268 ture possessing contiguously positioned beta-aminoethyl side chain, a set of three adjacent bromines,

269 nalogs bearing a C-methyl substituent on the aminoethyl side chain, exhibited reduced potency relativ

270 and conversion of the ester moiety to a beta-aminoethyl side chain.

271 eptoid is a 36-mer that contains 12 cationic aminoethyl side chains.

272 Derivatives with various aminomethyl and aminoethyl substituents on the para position of the C-2

273 ical procedure involves the treatment of a 1-aminoethyl-substituted butadiene with maleic anhydride a

274 evelopment of the domino reaction between an aminoethyl-substituted diene and maleic anhydride to aff

275 ed by the histamine H1 receptor agonist 2-(2-aminoethyl) thiazole dihydrochloride (10 microM) and blo

276 functionalized with the 2-(N-formyl-N-methyl)aminoethyl thiophosphate protecting group (CpG ODN fma15

277 s, the thermolytic 2-[N-methyl-N-(2-pyridyl)]aminoethyl thiophosphate protecting group is lost to a l

278 molytic cleavage of the 2-(N-formyl-N-methyl)aminoethyl thiophosphate protecting group.

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