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 results showed that the fish oil was rich in monomethyl and dimethyl furan fatty acids (c = 1.3 g/100

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

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

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

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

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

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

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

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

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

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

28 L-NG monomethyl arginine induced greater constriction in pati

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

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

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

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

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

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

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

36 resulted in a partial methylation producing monomethyl arsenic (MMA) and dimethyl arsenic (DMA).

37 Inorganic As (InAs) is methylated to monomethyl-arsenical species (MMAs) and dimethyl-arsenic

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

39 of cytotoxic drugs 5-fluorouracil (5-FU) and monomethyl auristatin E (MMAE) are partially activated b

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

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

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

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

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

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

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

47 Here, model drug monomethyl auristatin E (MMAE) was conjugated ex vivo to

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

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

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

51 Cytotoxicity of Monomethyl Auristatin E (MMAE)-EGFR-Pep11 peptide-drug c

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

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

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

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

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

57 2, but delivered the same cytotoxic payload (monomethyl auristatin E, MMAE), and we found that the in

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

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

60 ibody linked to the potent antimitotic agent monomethyl auristatin E.

61 antibody conjugated to the potent cytotoxin monomethyl auristatin E.

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

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

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

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

66 o the cytotoxic microtubule-disrupting agent monomethyl auristatin E.

67 y) and a substrate with the caged cytotoxic (monomethyl auristatin E: MMAE; a high-affinity tubulin l

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

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

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

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

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

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

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

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

76 y of pHLIP to deliver the cytotoxic compound monomethyl-auristatin-F to HeLa cells is increased sever

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

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

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

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

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

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

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

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

85 Speciated urinary arsenic (As) (inorganic + monomethyl + dimethyl As) was measured by high-performan

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

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

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

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

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

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

92 = 10, K(E) being the acidity constant of the monomethyl ester of 1, indicated the formation of an int

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

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

95 These monomethyl ester precursors were synthesized from the kn

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

123 Systemic administration of monomethyl fumarate, another agonist of the nicotinic ac

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

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

126 Diroximel fumarate is metabolised to monomethyl fumarate, the active metabolite of dimethyl f

127 Furthermore, the influence of an added monomethyl furan fatty acid 9-(3-methyl-5-pentylfuran-2-

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

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

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

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

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

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

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

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

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

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

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

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

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

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

142 etitive transgenic arrays and reduced global monomethyl H3K9 levels.

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

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

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

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

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

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

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

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

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

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

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

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

155 [4-benzoic acid]) porphyrin and l -NMMA (NG-monomethyl-l -arginine), a superoxide dismutase mimetic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

195 titive nitric oxide synthase inhibitor N(G) -monomethyl-l-arginine (l-NMMA, 5 mg kg(-1) bolus & subse

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

252 asymmetric dimethylarginine (ADMA) and N(G)-monomethyl-l-arginine, in tumor-bearing mice compared wi

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 efined as the inverse of FBF reserve to N(G)-monomethyl-L-arginine.

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

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

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

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

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

266 me degree by the NO synthase inhibitor N:(G)-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 ors asymmetrical dimethylarginine (ADMA) and 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 l furan fatty acids degraded faster than the monomethyl ones, but also faster than tocopherols.

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

290 The median concentrations of 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