ライフサイエンスコーパス: aminoethyl

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 BTAs 3 and 4 are linked to 5-(2-aminoethyl)-2-iminoimidazolidin-4-one and a hexahydropyr

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

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

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

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

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

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

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

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

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

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

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

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

28 5'-S-(2-aminoethyl)-6-N-(4-nitrobenzyl)-5'-thioadenosine (SAENTA

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

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

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

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

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

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

35 amino acid (MPAA) ligands or mono-protected aminoethyl amine (MPAAM) ligands.

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

37 his LbL method uses a small molecule, tris(2-aminoethyl) amine (TAEA), and a colloidal dispersion of

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

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

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

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

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

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

44 t covalent framework by incorporating tris(2-aminoethyl)amine (TREN).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

73 ylimidodicarbonate is demonstrated as a beta-aminoethyl anion synthetic equivalent.

74 oparticles (NPs) modified with the PEGylated aminoethyl anisamide (AEAA, a targeting ligand for sigma

75 lidate the therapeutic potential, we utilize aminoethyl anisamide-conjugated lipid-calcium-phosphate

76 se conjugates containing a guanidinoethyl or aminoethyl auxiliary pendant on the cyclen moiety was de

77 The Ser protease inhibitor AEBSF (4-[2-aminoethyl] benzene sulfonyl fluoride) up-regulated full

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

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

80 ydrase II (CAII) binding to immobilized 4-(2-aminoethyl)benzenesulfonamide (AEBSA) to examine the eff

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

97 4-(2-Aminoethyl)-benzenesulfonyl fluoride, a specific inhibit

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

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

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

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

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

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

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

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

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

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

108 ionalized oligothiophene cations, i.e., (bis-aminoethyl)bithiophene, through a collective influence o

109 functionalized with 1H-imidazolium-1,3-bis(2-aminoethyl)bromide ionic liquid (IBABr) to prepare IBABr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

127 2-Aminoethyl diphenylborinate but not SKF-96365 abrogated

128 2-Aminoethyl diphenylborinate was recently identified as a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

152 electrode array (MEA) functionalized with (2-aminoethyl)ferrocene (AEF) tagged specific peptide subst

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

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

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

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

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

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

159 a) of three consecutive PNA monomers of N-(2-aminoethyl)glycine (aeg) scaffolds (the sequential archi

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

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

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

163 om Escherichia coli O36 in the form of its 2-aminoethyl glycoside is reported.

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

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

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

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

168 -1-phenylethyl and 2-[N-methyl-N-(2-pyridyl)]aminoethyl groups are particularly promising for 5'-hydr

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

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

171 9-[N-(2-carboxyethyl)-N-(2-phosphonoethyl)-2-aminoethyl]guanine has a K(i) of 50 nM, the best inhibit

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

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

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

175 agment compared with 4,6-dichloro-2-methyl-3-aminoethyl-indole (DCAI), a Ras ligand previously descri

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

201 2-Aminoethyl methanethiosulfonate (MTSEA(+)) failed to mod

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

227 2-(Aminoethyl)methanethiosulfonate hydrobromide (MTSEA) fai

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

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

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

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

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

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

234 2-(Aminoethyl)-methanethiosulfonate hydrobromide (MTSEA)-bi

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

236 3C or T47C substitutions were sensitive to 2-aminoethyl methanethiosulphonate (MTSEA) modification.

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

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

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

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

241 2-Aminoethyl methylphosphonate (2-AEMP), an analog of GABA

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

269 a derivative, prepared by reacting 2-[(1R)-1-aminoethyl]phenol with benzoyl isothiocyanate, constitut

270 Thiourea derivatives of 2-[(1R)-1-aminoethyl]phenol, (1S,2R)-1-amino-2,3-dihydro-1H-inden-

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

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

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

274 21680 (4-((N-ethyl-5'-carbamoyladenos-2-yl)-aminoethyl)-phenylpropionic acid) had no effect.

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

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

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

278 (2-), 1-aminoethyl phosphonate [1AEP](2-), 2-aminoethyl phosphonate [2AEP](2-), aminopropyl phosphona

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

280 By incorporating 1-(2-aminoethyl)piperazine (AEPIP) into a commercial epoxy bl

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

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

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

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

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

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

287 accessed the latter via the addition of a 2-aminoethyl side chain onto a lactam moiety.

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

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

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

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

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

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

294 n, relationships between the structures of 1-aminoethyl-substituted chromenes and their antimalarial

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

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

297 Herein we report a monoprotected aminoethyl thioether (MPAThio) ligand-enabled beta-C(sp(

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

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

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