ライフサイエンスコーパス: monomethyl

1 These 3-monomethyl-1-alkanols were then converted to two stereoi

2 nzyloxy)-9H-purin-2-yl)carbamate (1) and its monomethyl (2) and gem-dimethyl analogues (3), were test

3 identified novel H3 K18 methylation, H3 K27 monomethyl/acetyl duel modifications, H2B K23 acetylatio

4 compounds remaining after leaving out small monomethyl alkanes.

5 c acid, squalene, monoethanol amine sulfate, monomethyl amine sulfate, and two sources of humic acid,

6 eric monomethoxy analogues (3-6), 4 isomeric monomethyl analogues (7-10), 4 4-alkyl/aryl-substituted

7 e suvh4 suvh5 suvh6 triple mutant loses both monomethyl and dimethyl H3 K9 at target loci.

8 Herein, we report the ability of five monomethyl and five carbomethoxymethyl derivatives of qu

9 e complexes with hydroquinone diesters yield monomethyl and monoethyl derivatives of acetylhydroquino

10 ration of well-defined (pyridine-pyrrolyl)Ni monomethyl and monophenyl complexes that allow the direc

11 d to histone H4 peptides bearing unmodified, monomethyl, and dimethyl Lys-20 reveal that the phenylal

12 f dLsd1 strongly affects the global level of monomethyl- and dimethyl-H3-K4 methylation and results i

13 alian ortholog has been shown to demethylate monomethyl- and dimethyl-K4 and -K9 residues of histone

14 crystal structures of L3MBTL1 complexes, the monomethyl- and dimethyllysines insert into a narrow and

15 Monomethyl- and dimethylphosphoethanolamine are detected

16 , CONHNH2, CN, or CN4H (tetrazole), only the monomethyl- and N,N-dimethylamides proved to be active.

17 gulation in multiple RNA pathways, including monomethyl- and trimethylguanosine-capped RNAs.

18 relatively selective iNOS inhibitor), L-N(G)-monomethyl arginine (an isoform-nonselective NO synthase

19 ine (L-NMMA) (NOS inhibitor) but not of D-NG-monomethyl arginine (D-NMMA) (L-NMMA-inactive enantiomer

20 e), and it decreased in the presence of L-NG-monomethyl arginine (L-NMMA) (NOS inhibitor) but not of

21 onary infusions of acetylcholine (ACH), L-NG monomethyl arginine (L-NMMA) and sodium nitroprusside.

22 Asymmetric dimethylarginine (ADMA) and monomethyl arginine (L-NMMA) are endogenously produced a

23 Non specific inhibitors of iNOS, L-NG-monomethyl arginine (L-NMMA), and L-arginine-methyl este

24 pre-treatment with the NOS inhibitor, L-N(G)-monomethyl arginine (L-NMMA, 1 mM).

25 Although all PRMTs produce monomethyl arginine (MMA), type 1 PRMTs go on to form as

26 inhibitable by the NO synthase inhibitors L-monomethyl arginine and L-N(6)-(1-iminoethyl) lysine dih

27 N-Acetylcysteine, catalase, and l-N(G)-monomethyl arginine citrate inhibited the ROS/RNS fluore

28 L-NG monomethyl arginine decreased platelet cGMP content to a

29 L-NG monomethyl arginine induced greater constriction in pati

30 We also show that heat and L-N(G)-monomethyl arginine reduce the mitotic indices of primar

31 bits NO accumulation by GCPs and that L-N(G)-monomethyl arginine, an inhibitor of NO production in an

32 ed by the addition of aminoguanidine, L-N(G)-monomethyl arginine, or Tiron.

33 uppressed mitosis in mesangial cells by an L-monomethyl arginine-inhibitable mechanism.

34 P) and basal nitric oxide activity with L-NG monomethyl arginine.

35 not affected by the NO synthase inhibitor NG-monomethyl- -arginine (NGMA).

36 he specific inhibitor of NO synthase, N(G)-l-monomethyl-arginine (l-NMMA) or by a combination of wort

37 zyme that citrullinates histone arginine and monomethyl-arginine residues thereby regulating histone

38 amino acid and hydroxylamine functionalized monomethyl auristatin D with either protease-cleavable o

39 fects of the microtubule destabilizing agent monomethyl auristatin E (MMAE) conjugated to the humaniz

40 body cAC10, linked to the antimitotic agents monomethyl auristatin E (MMAE) or F (MMAF), produces pot

41 o, were conjugated with the cytotoxic agents monomethyl auristatin E (MMAE) or monomethyl auristatin

42 cacy of ADCs with VC(S) linkers armed with a monomethyl auristatin E (MMAE) payload.

43 that nanoparticle-drug conjugates (NDCs) of monomethyl auristatin E (MMAE) significantly increase lo

44 by conjugating to cAC10 the cytotoxic agent monomethyl auristatin E (MMAE) to create the antibody-dr

45 CD30-directed therapy, the antitubulin agent monomethyl auristatin E (MMAE) was attached to a CD30-sp

46 We hypothesized that the anti-tubulin agent monomethyl auristatin E (MMAE), a component of a clinica

47 ite-specifically conjugated duocarmycin- and monomethyl auristatin E (MMAE)-based anti-PSMA ADCs with

48 rotein is a promising target for antimitotic monomethyl auristatin E (MMAE)-based antibody-drug conju

49 Auristatin F (mcMMAF) and valine-citrulline-monomethyl Auristatin E (vcMMAE) at interchain cysteine

50 ading, a lysosomal release functionality and monomethyl auristatin E as a cytotoxic payload.

51 y sequence of the ADC conjugated with either monomethyl auristatin E or F (vcMMAE/mcMMAF) displayed t

52 When conjugated to monomethyl auristatin E, an antibody against the ovarian

53 ug conjugate (ADC) that selectively delivers monomethyl auristatin E, an antimicrotubule agent, into

54 2, but delivered the same cytotoxic payload (monomethyl auristatin E, MMAE), and we found that the in

55 a monoclonal antibody (cAC10) conjugated to monomethyl auristatin E, targets CD30(+) receptors.

56 Brentuximab vedotin is a monomethyl auristatin E-conjugated monoclonal antibody d

57 antibody conjugated to the potent cytotoxin monomethyl auristatin E.

58 njugated to the microtubule-disrupting agent monomethyl auristatin E.

59 tibody, conjugated via a cleavable linker to monomethyl auristatin E.

60 oprotein NMB (gpNMB) to the potent cytotoxin monomethyl auristatin E.

61 le linker to a microtubule-disrupting agent, monomethyl auristatin E.

62 f IgG1 mAbs conjugated with maleimidocaproyl-monomethyl Auristatin F (mcMMAF) and valine-citrulline-m

63 xic agents monomethyl auristatin E (MMAE) or monomethyl auristatin F (MMAF).

64 able ADCs carrying the structurally distinct monomethyl auristatin F were unaffected by SLC46A3 atten

65 atin phenylalanine phenylenediamine (AFP) or monomethyl auristatin phenylalanine (MMAF), two novel de

66 t with E-selectin antibody valine-citrulline monomethyl-auristatin E in vivo, with more than 85% inhi

67 (ADC), E-selectin antibody valine-citrulline monomethyl-auristatin E, was a potent and selective agen

68 with the anticancer drug N-phenyl maleimide monomethyl-auristatin-E (MMAE) maintained high cytotoxic

69 to antimitotic agents such as paclitaxel and monomethyl-auristatin-E (MMAE).

70 Rv generates a mutant incapable of producing monomethyl branched unsaturated C(16) to C(20) fatty aci

71 opment shortly after hatching in response to monomethyl branched-chain fatty acid (mmBCFA) deficiency

72 r in Caenorhabditis elegans development, the monomethyl branched-chain fatty acid C17ISO, a product o

73 We previously showed that leucine-derived monomethyl branched-chain fatty acids (mmBCFAs) and deri

74 Here, we show that monomethyl branched-chain fatty acids (mmBCFAs) and thei

75 DH may also be required for the synthesis of monomethyl branched-chain fatty acids (mmBCFAs) from BCA

76 onstrates that the schistosome protein binds monomethyl cap in a manner similar to that of single spe

77 wed by selective formation of ethane and the monomethyl complex (N4)Pd(II)Me(OH).

78 abluB strain to convert Mg-protoporphyrin IX monomethyl ester (MPE) into protochlorophylide, a reacti

79 Surprisingly, Mg-protoporphyrin IX monomethyl ester (oxidative) cyclase, AcsF, was identifi

80 ytochrome f, diiron magnesium protoporphyrin monomethyl ester cyclase, and Fe2S2-containing ferredoxi

81 act mass spectrum as one of the two possible monomethyl ester derivatives of (2R,3S)-3-isopropylmalat

82 g-protoporphyrin IX and Mg-protoporphyrin IX monomethyl ester in the PS I-less/ch/L-/scpE- strain, wh

83 electively protected N,S-ditritylglutathione monomethyl ester is described involving the chemical mod

84 = 10, K(E) being the acidity constant of the monomethyl ester of 1, indicated the formation of an int

85 nd the acyl cyano or bromo derivative of the monomethyl ester of 3,7-dimethyl-2,4,6-octatriene-1,8-di

86 g reporter plasmids for Mg-protoporphyrin IX monomethyl ester oxidative cyclase (bchE), Mg-protoporph

87 These monomethyl ester precursors were synthesized from the kn

88 rebs cycle intermediates, only succinic acid monomethyl ester specifically stimulated proinsulin bios

89 rotochlorophyllide from Mg-protoporphyrin IX monomethyl ester, Ho1 oxidatively cleaves heme to form b

90 f Crd1/CHL27 accumulate Mg-protoporphyrin IX monomethyl ester, the substrate of the cyclase reaction.

91 the bacterium Escherichia coli catalyzes the monomethyl esterification of trans-aconitate and related

92 This enzyme catalyzes the monomethyl esterification of trans-aconitate at high aff

93 onitate methyltransferase also catalyzes the monomethyl esterification of trans-aconitate, we identif

94 ting/accepting site, using protoporphyrin IX-monomethyl esters (PPIX(MME)) and N-methylimidazole (MeI

95 ing was exploited to prepare phosphonic acid monomethyl esters in high yield by transesterification i

96 The beta-hydroxy phosphonic acid monomethyl esters were dehydrated with diisopropylcarbod

97 oxins: aflatoxin B1 (50 mug/kg), alternariol monomethyl ether (<LOQ - 79 mug/kg), alternariol (303-35

98 = Et, t-Bu, i-Am; n = 1-3) and thiodiethanol monomethyl ether (9) have been synthesized and used as b

99 ncing estrogenicity (as seen for alternariol monomethyl ether (AME)) while hydroxylation and glucuron

100 detection of alternariol (AOH), alternariol monomethyl ether (AME), altenuene (ALT), tentoxin (TEN),

101 ycotoxins, alternariol (AOH) and alternariol monomethyl ether (AME), has been investigated during the

102 cid (TeA), alternariol (AOH) and alternariol monomethyl ether (AME), in whole wheat flour were invest

103 ycotoxins, alternariol (AOH) and alternariol monomethyl ether (AME), were synthesized and applied to

104 arged sodium adducts of poly(ethylene oxide) monomethyl ether (CH3O-PEO-H) for positive ionization in

105 d ranged from 0.3 to 50.5 mug/g, alternariol monomethyl ether from 0.5 to 32.3 mug/g, while tentoxin

106 chloroisobutyrate-poly(oligo(ethylene oxide) monomethyl ether methacrylate)-b-poly(n-butyl methacryla

107 itions with a monomer, oligo(ethylene oxide) monomethyl ether methacrylate, efficiently producing a p

108 ernaria mycotoxins (alternariol, alternariol monomethyl ether, and tentoxin) in pomegranate samples (

109 at a hydrolysis byproduct, diethylene glycol monomethyl ether, is likely a contributing factor.

110 e, triethyl phosphate, and dipropyleneglycol monomethyl ether, were collected from an Ion Track ITEMI

111 s of bromide and aromatization to resorcinol monomethyl ethers of defined substitution pattern.

112 particular, some gallamides and pyrogallol-1-monomethyl ethers showed remarkable affinity and selecti

113 ) inhibitor complexes bound to tri-, di- and monomethyl forms of H3K9 and the trimethyl form of H3K36

114 tem (CNS) tissue is predominantly exposed to monomethyl fumarate (MMF), the bioactive metabolite of D

115 DMF and, more so, its active metabolite, monomethyl fumarate, are known agonists of the hydroxyca

116 They also show that the antipsoriasis drug monomethyl fumarate, itself a GPR109A agonist, provokes

117 anscribed genes in a 5'-to-3' tri- to di- to monomethyl gradient and promotes association of chromati

118 vity is as follows: trimethyl- > dimethyl- > monomethyl- > TCEP >> DTT; tmTCEP is 35-fold more reacti

119 However, the male is positive for monomethyl H3-K9 and H3-K27 and these signals increase d

120 Recent evidence identifies monomethyl H3-K9 as the preferred substrate of Suvar39h,

121 The association of HP1beta with monomethyl H3-K9 may assist in preventing further modifi

122 - and trimethyl H3-K9, and co-localises with monomethyl H3-K9.

123 lzf-expressing spermatogonia completely lack monomethyl-H3-K27 and monomethyl-H4-K20, and contain ver

124 d monomethyl-H4-K20, and contain very little monomethyl-H3-K9.

125 Effect of high glucose on monomethyl H3K4 (H3K4me1), dimethyl H3K4 (H3K4me2), and

126 tant (Kd) of approximately 5 microm, whereas monomethyl H3K4 binds CHD1 with a 3-fold lower affinity.

127 al differentiation between dimethyl H3K4 and monomethyl H3K4, with the latter operating as an epigene

128 observations are consistent with a role for monomethyl H3K9 as an epigenetic mark of repressed chrom

129 tivation correlated with the partial loss of monomethyl H3K9 from their chromatin.

130 Yet, the biological significance of monomethyl H3K9 has remained unclear because of the lack

131 etitive transgenic arrays and reduced global monomethyl H3K9 levels.

132 ogonia completely lack monomethyl-H3-K27 and monomethyl-H4-K20, and contain very little monomethyl-H3

133 Here, we present Hg speciation (monomethyl-Hg) and stable isotopic composition (C, N, Hg

134 ibodies recognizing SMEDWI-1 and Histone H4 (monomethyl-K20) and cell-cycle markers to label subsets

135 which was suppressed by the addition of N(G)-monomethyl L-arginine (NMMA), an inhibitor of inducible

136 of the l-arginase-nitric oxide pathway (N(G)-monomethyl l-arginine [l-NMMA] monoacetate) reversed the

137 Preexposure to N(G)-monomethyl L-arginine acetate (L-NMMA), a nitric oxide s

138 N(G)-monomethyl L-arginine completely inhibited the increase

139 ng that the frequently used NOS inhibitor NG-monomethyl L-arginine enhanced O-2 production in the pre

140 es with a soluble inhibitor of nitric oxide (monomethyl l-arginine) and by showing the absence of E(2

141 th the nitric oxide synthase inhibitor (N(G)-monomethyl L-arginine).

142 asymmetric dimethylarginine (ADMA) and N (G)-monomethyl- l-arginine (L-NMMA) regulate nitric oxide (N

143 ibition via intra-arterial infusion of N(G) -monomethyl-L -arginine (L -NMMA) into the common femoral

144 Using an intra-arterial infusion of N(G) -monomethyl-L -arginine (L -NMMA) to inhibit nitric oxide

145 Specifically, administration of NG-monomethyl-l -arginine (NGMMA) via osmotic pumps increas

146 [4-benzoic acid]) porphyrin and l -NMMA (NG-monomethyl-l -arginine), a superoxide dismutase mimetic

147 (1 microM) or the NO synthase inhibitor N(G)-monomethyl-L-arginine (10 microM) was added before TNF-a

148 n with a nitric oxide synthase inhibitor, NG-monomethyl-L-arginine (10 or 100 micromol l-1), nor the

149 In contrast, N(G)-monomethyl-L-arginine (2 micromol/min) infusion reduced

150 The nonselective NOS inhibitor N(G)-monomethyl-L-arginine (25 micromol/min) also reduced bas

151 of the nitric oxide synthesis inhibitor N:(G)monomethyl-L-arginine (5.3+/-1.2% versus 0.7+/-0.7%, P:<

152 -L-arginine methyl ester (30 microm) or N(G)-monomethyl-L-arginine (50 microm), by beta-adrenoceptor

153 NG-monomethyl-L-arginine (L-NMA) potentiated the increase i

154 ), and/or the NO synthase (NOS) inhibitor NG-monomethyl-L-arginine (L-NMMA) (0.1 mmol/l).

155 and absence of the NO synthase antagonist NG-monomethyl-l-arginine (l-NMMA) (0.3 mg/kg/min intravenou

156 of the nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine (L-NMMA) (3 mg kg(-1)) or increasi

157 NO synthase inhibitor N(G)-monomethyl-L-arginine (L-NMMA) abolished stimulated NO p

158 Inhibition of NO synthase with N(G)-monomethyl-L-arginine (L-NMMA) affected neither the decl

159 the nitric oxide (NO) synthase inhibitor N G-monomethyl-L-arginine (L-NMMA) after stellate block virt

160 after 2 h (but not 1 h) was abolished by NG-monomethyl-l-arginine (l-NMMA) and 2-amino-5,6-dihydro-6

161 O) synthase inhibitors (20 micromol l-1) N G-monomethyl-L-arginine (L-NMMA) and N G-nitro L-arginine

162 relaxations similarly in both groups, but NG-monomethyl-L-arginine (L-NMMA) did not inhibit relaxatio

163 r blockade of forearm NO synthesis with N(G)-monomethyl-L-arginine (L-NMMA) followed by forearm exerc

164 ide generation with subpressor doses of N(G)-monomethyl-L-arginine (L-NMMA) in C57B6 and Tie-2/green

165 Intra-arterial infusion of N(G)-monomethyl-L-arginine (L-NMMA) increased iliac PWV signi

166 The nitric oxide synthase inhibitor N(G)-monomethyl-l-arginine (l-NMMA) inhibited l-arginine's ef

167 ne methyl ester hydrochloride (L-NAME) or NG-monomethyl-L-arginine (L-NMMA) reduced the increase in D

168 asymmetric dimethylarginine (ADMA) and N(G)-monomethyl-L-arginine (L-NMMA) regulate nitric oxide (NO

169 ction of the nonselective NOS inhibitor N(G)-monomethyl-l-arginine (l-NMMA) slowed the recovery to eu

170 ulate vascular endothelial dysfunction, N(G)-monomethyl-L-arginine (L-NMMA) was infused into the brac

171 arterial infusions of acetylcholine and N(G)-monomethyl-L-arginine (L-NMMA) were used to assess stimu

172 ll wal1-induced arthritis in rats with N:(G)-monomethyl-L-arginine (L-NMMA), a competitive nonspecifi

173 NOS activity in p47(phox-/-) mice using N(G)-monomethyl-L-arginine (L-NMMA), a large proportion of th

174 ndiabetic rats after pretreatment with N:(G)-monomethyl-L-arginine (L-NMMA), a nitric oxide synthase

175 is study, we investigated the effect of N(G)-monomethyl-L-arginine (L-NMMA), a nonspecific NOS inhibi

176 e and after intra-arterial infusions of N(G)-monomethyl-l-arginine (L-NMMA), TEA, fluconazole, and th

177 (n=12), saline; group 2 (n=9), 3 mg/kg N(G)-monomethyl-L-arginine (L-NMMA), which crosses the blood-

178 FFA elevation blunted the LBF response to NG-monomethyl-L-arginine (L-NMMA), which is an inhibitor of

179 on plethysmography using acetylcholine and N-monomethyl-L-arginine (L-NMMA), with sodium nitroprussid

180 (control) and the NO synthase inhibitor N(G)-monomethyl-L-arginine (L-NMMA).

181 en with nitric oxide synthase inhibitor N(G)-monomethyl-l-arginine (l-NMMA).

182 roprusside, and the NO synthase inhibitor NG-monomethyl-L-arginine (L-NMMA).

183 ) without and with coadministration of N:(G)-monomethyl-L-arginine (L-NMMA).

184 re and following topical application of N(G)-monomethyl-L-arginine (L-NMMA).

185 rial infusion of the NO synthase inhibitor N-monomethyl-L-arginine (L-NMMA).

186 hibition via intra-arterial infusion of N(G)-monomethyl-L-arginine (L-NMMA).

187 cetylcholine, sodium nitroprusside, and N(G)-monomethyl-L-arginine (L-NMMA).

188 using the nitric oxide synthase inhibitor NG-monomethyl-L-arginine (L-NMMA); and nitroprusside was us

189 with the nitric oxide synthase inhibitor NG-monomethyl-l-arginine (l-NMMA, 10 mm), the non-selective

190 g IV), (2) the NO synthase inhibitor L-N:(G)-monomethyl-L-arginine (L-NMMA, 4 micromol/min intra-arte

191 min) with and without the NOS inhibitor N(G)-monomethyl-L-arginine (L-NMMA, 5 mg/min).

192 gonists that stimulate NO production) and NG-monomethyl-L-arginine (L-NMMA, an inhibitor of NO produc

193 ith the nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine (L-NMMA; 100 microM) significantly

194 NOS inhibition with N(G)-monomethyl-L-arginine (L-NMMA; 20 mg/kg) had no effect o

195 tracoronary NO synthase inhibition with N(G)-monomethyl-L-arginine (L-NMMA; 25 micromol/min) on basal

196 responses to intra-arterial infusions of NG-monomethyl-l-arginine (l-NMMA; an inhibitor of NO syntha

197 were not restored by NOS inhibition with NG-monomethyl-L-arginine (L-NMMA; n = 6) or NG-nitro-L-argi

198 le nitric oxide synthase (iNOS) inhibitor NG-monomethyl-L-arginine (NGMMLA) or the H2O2 scavenger cat

199 usion of the nonselective NOS inhibitor N(G)-monomethyl-L-arginine (NMA) on skeletal muscle postcapil

200 se to AA was blocked by incubation with N(G)-monomethyl-l-arginine (NMMA) (300 microM), a competitive

201 ition of iNOS gene expression by use of N(G)-monomethyl-L-arginine (NMMA) inhibited apoptosis, wherea

202 to L-citrulline, but the NOS inhibitor N(G)-monomethyl-L-arginine (NMMA) inhibited this reaction.

203 uracil incorporation by T. gondii, and N(G)-monomethyl-L-arginine (NMMA) treatment did not reverse t

204 An inhibitor of NO synthase (NOS), N(G)-monomethyl-l-arginine (NMMA), prevented the increase in

205 r a nitric oxide synthase (NOS) inhibitor (N-monomethyl-L-arginine (NMMA); 300 or 500 microM) or a so

206 e responses were significantly attenuated by monomethyl-l-arginine (P<0.01 versus placebo).

207 Similarly, NG-monomethyl-L-arginine 1 mmol/L and NG-nitro-L-arginine 1

208 ygenases (fluconazole) and NO synthase (N(G)-monomethyl-l-arginine [L-NMMA]).

209 ioavailability (percent constriction to N(G)-monomethyl-l-arginine [mean (SEM) wild type 106% (30%);

210 The nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine abolished augmentation of the meth

211 f the nitric oxide synthase inhibitor l-N(G)-monomethyl-l-arginine acetate (l-NMMA) into both femoral

212 ion (P=0.01) but not further increased by NG-monomethyl-L-arginine acetate (P=0.2).

213 mice had increased plasma levels of ADMA and monomethyl-l-arginine and reduced endothelial nitric oxi

214 of the nitric oxide synthase inhibitor, N(G)-monomethyl-L-arginine at a concentration of 10 mM (n = 7

215 , and inhibition of the NO synthase by N (G)-monomethyl-L-arginine attenuated but did not completely

216 The NO synthase inhibitor N-monomethyl-L-arginine blocked the inhibitory Arg effect

217 ction by activated macrophages by using N(G)-monomethyl-L-arginine blocks their production of ONOO(-)

218 However, H(2)O(2) and N(omega)-monomethyl-l-arginine could induce HLA-DRA expression su

219 treatment of mice with the NOS inhibitor NG-monomethyl-l-arginine delayed weight loss and death amon

220 infusion of the nitric oxide inhibitor N(G)-monomethyl-L-arginine during SS euglycemic hyperinsuline

221 Mtb infection, and inhibition of NO by N(G)-monomethyl-L-arginine enhanced intracellular survival of

222 N(G)-monomethyl-L-arginine fails to prevent poly IC- and poly

223 injection of the NO synthase inhibitor N(G)-monomethyl-l-arginine in healthy volunteers resulted in

224 Nonetheless, the iNOS inhibitor N(G)-monomethyl-L-arginine inhibited IFN-gamma-mediated intra

225 diated by enhanced NO activity, because N(G)-monomethyl-l-arginine markedly blunted the flow response

226 s, elevated adenosine triphosphate, and N(G)-monomethyl-L-arginine monoacetate did not affect the rat

227 Neither N(G)-monomethyl-l-arginine nor diphenyleneiodonium chloride a

228 The inhibition by N(G)-monomethyl-L-arginine of VEGF-induced HUVEC migration an

229 endogenous NO synthase activity by N(omega)-monomethyl-l-arginine or addition of exogenous hydrogen

230 vity with the nonspecific NOS inhibitor N(G)-monomethyl-L-arginine or by the antioxidants N-acetyl-L-

231 hesis was inhibited by the NOS inhibitors NG-monomethyl-L-arginine or N-3-aminoethylbenzylacetamidine

232 The addition of N(G)-monomethyl-L-arginine protected against lipopolysacchari

233 uld be largely prevented by addition of N(G)-monomethyl-L-arginine to inhibit nitric oxide (NO) gener

234 N(G)-monomethyl-l-arginine was administered to a subgroup of

235 onstrictor response to NO inhibition by N(G)-monomethyl-L-arginine was significantly higher after ins

236 cient mice treated with the iNOS inhibitor N-monomethyl-l-arginine were largely unable to resolve gen

237 nary artery diameter, and the effect of N(G)-monomethyl-l-arginine were similar between the groups at

238 eincubation of myocytes in 1 mM L-NMMA (N(G)-monomethyl-L-arginine) + 1 mM L-NNA (N(G)-nitro-L-argini

239 nitric oxide synthase inhibitor l-NMMA (N(G)-monomethyl-l-arginine) indicated that (*)NO influenced t

240 he nitric oxide synthase inhibitor L-NAME (N-monomethyl-L-arginine) or the xanthine oxidase inhibitor

241 he synthesis of nitric oxide, and L-NMMA (NG-monomethyl-L-arginine), a nitric oxide synthase blocker,

242 of inhibitors of inducible NO synthase (N(G)-monomethyl-L-arginine), as well as anti-IFN-gamma Abs, r

243 rease was blocked by the NOS inhibitor (N(G)-monomethyl-L-arginine), but could be restored by the add

244 t with a competitive inhibitor of eNOS (N(G)-monomethyl-L-arginine, 10(-3) mol/L).

245 ned with intradermal microdialysis of l-N(G)-monomethyl-l-arginine, a nitric oxide antagonist, in res

246 Conversely, N(G)-monomethyl-L-arginine, a NOS inhibitor, decreased PPARga

247 Furthermore, N-monomethyl-L-arginine, an inhibitor of iNOS, completely

248 lpha was lost either after treatment with NG-monomethyl-l-arginine, an inhibitor of NO production, or

249 PVL-20G and RAL rats was corrected by N(G)()-monomethyl-L-arginine, and nitric oxide synthase enzyme

250 ric oxide synthase, aminoguanidine, and N(G)-monomethyl-L-arginine, attenuate poly IC + IFN-gamma-ind

251 ibition of nitric oxide synthase by N(gamma)-monomethyl-L-arginine, blood flow responses did not diff

252 or by the nitric oxide synthase inhibitor NG-monomethyl-l-arginine, fluorescence recovery was signifi

253 olamine and yohimbine), and nitric oxide (NG-monomethyl-L-arginine, L-NMMA) regulation of blood flow.

254 de coupled with NO synthase inhibition (N(G)-monomethyl-L-arginine, L-NMMA).

255 out the nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine, monoacetate salt (L-NMMA).

256 A-DCs was blocked by the iNOS inhibitor N(G)-monomethyl-l-arginine, monoacetate salt, and 3) RA-DCs d

257 st opsonized rickettsiae was inhibited by NG-monomethyl-L-arginine, superoxide dismutase, catalase, o

258 by opsonized rickettsiae was inhibited by NG-monomethyl-L-arginine, superoxide dismutase, mannitol, o

259 n response to the NO synthase inhibitor N(G)-monomethyl-l-arginine, was reduced in IRKO (61 +/- 14 vs

260 as blocked by the NO synthase inhibitor N(G)-monomethyl-L-arginine.

261 g specific inhibition of NO synthase by N(G)-monomethyl-L-arginine.

262 lyceryl trinitrate, norepinephrine, and l-NG-monomethyl-l-arginine.

263 of NO because it was entirely inhibited by N-monomethyl-L-arginine.

264 the nitric oxide synthase (NOS) inhibitor NG-monomethyl-l-arginine.

265 me degree by the NO synthase inhibitor N:(G)-monomethyl-L-arginine.

266 ors asymmetrical dimethylarginine (ADMA) and monomethyl-l-arginine.

267 itor NG-nitro-L-arginine methyl ester and NG-monomethyl-L-arginine.

268 de (NO) was seen that could be blocked by NG-monomethyl-L-arginine.

269 t not GTN on IP(DVP) were attenuated by N(G)-monomethyl-L-arginine.

270 (DETA-NO), and the NO synthase inhibitor, NG-monomethyl-L-arginine.monoacetate (L-NMMA), showed that

271 bined blockade of NO synthase (NOS; via N(G)-monomethyl-L-arginine: L-NMMA) and cyclooxygenase (COX;

272 ion (control) and NO synthase inhibition (NG-monomethyl-L-arginine; L-NMMA) under normoxic and normoc

273 an inhibitor of nitric oxide synthase (N(G)-monomethyl-L-arginine; L-NMMA; 10 and 100 microM).

274 prostaglandins (BaCl2, ouabain, L-NMMA [N(G)-monomethyl-L-arginine] and ketorolac, respectively).

275 In the ventricular and subventricular zones, monomethyl-lysine 9 of H3 (H3K9me1) was decreased by 25%

276 arks are strongly reduced or absent, and the monomethyl mark is significantly increased.

277 study characterized distribution patterns of monomethyl mercury (MeHg) and areal mass of total mercur

278 We measured total mercury (THg) and monomethyl mercury (MMHg) concentrations and mercury (Hg

279 We show 2008 seasonal trends of total and monomethyl mercury (THg and MeHg, respectively) in herbi

280 erting MAs(V) into the more toxic metabolite monomethyl monothioarsenate (MMMTAs(V)), and transformed

281 were coated with the polymer - N-palmitoyl-N-monomethyl-N,N-dimethyl-N,N,N-trimethyl-6-O-glycolchitos

282 nitric-oxide synthase (NOS) inhibitors N(G)-monomethyl-N-arginine monoacetate (l-NMMA) and 1400W.

283 n headgroup as well as to those possessing 2-monomethyl or 2,2-dimethyl substituents.

284 for the first time of ethane formation from monomethyl Pd complexes.

285 es with O2 to produce a highly electrophilic monomethyl Pd(IV) transient that is involved in subseque

286 tidylcholine, phosphatidylethanolamine (PE), monomethyl PE, and dimethyl PE (PE-Me2) onto a glass sur

287 hate antigens (isopentenyl pyrophosphate and monomethyl phosphate).

288 We report that phosphinates as well as monomethyl phosphonates represent excellent isosters, wh

289 The median concentrations of monomethyl phthalate (mMP), monoethyl phthalate (mEP), m

290 to 14 (mean 10.42) were collected to measure monomethyl phthalate (MMP), monoethyl phthalate (MEP), m

291 -( 37) were prepared by methylation of their monomethyl precursors 16, 17, and 18, with [(11)C]iodome

292 </= 8, the reaction leads to a C1-symmetric monomethyl Pt(IV) complex (dpms)Pt(IV)Me(OH)2 (5) with h

293 The neutral (1 and 2) and monomethyl salts (3 and 4) undergo chemisorptive reactio

294 e that targets H3K36 modified in the di- and monomethyl state.

295 by functionality, (5) induce symmetry into a monomethyl substituted chiral center, and (6) apply the

296 Monomethyl succinate (MMS) combined with a barely stimul

297 Here, we show that monomethyl sulfate acts as an efficient alkylating agent

298 ive mitotic defects, including a switch from monomethyl to dimethyl lysine 20 of histone H4 (H4-K20)

299 is concept, scaffold monomers that contain a monomethyl triethyleneglycol branch were used to organiz

300 total urine As (uAs), and %uAs metabolites [monomethyl (%uMMA(V)), dimethyl (%uDMA(V)), and inorgani