ライフサイエンスコーパス: methanesulfonate

1 sensitivity to the DNA-damaging agent methyl methanesulfonate.

2 iae treated with the alkylating agent methyl methanesulfonate.

3 ive to treatment with mitomycin C and methyl methanesulfonate.

4 uced by camptothecin, hydroxyurea and methyl-methanesulfonate.

5 sitivity to the DNA-methylating agent methyl methanesulfonate.

6 with the DNA-damaging agents H2O2 and methyl methanesulfonate.

7 t with the DNA-damaging agents UV and methyl methanesulfonate.

8 e breast cancer cells' sensitivity to methyl methanesulfonate.

9 XRCC1-deficient CHO cells exposed to methyl methanesulfonate.

10 nd in HAT1 resulted in sensitivity to methyl methanesulfonate.

11 n was prepared by mutagenesis by using ethyl methanesulfonate.

12 bleomycin but not to damage caused by methyl methanesulfonate.

13 p53 expression in cells treated with methyl methanesulfonate.

14 zinc reagents derived from (S)-3-butyn-2-ol methanesulfonate.

15 sensitivity to the DNA-damaging agent methyl methanesulfonate.

16 MO was specifically induced during growth on methanesulfonate.

17 eprivation and DNA damage elicited by methyl methanesulfonate.

18 li to killing by the alkylating agent methyl methanesulfonate.

19 lume were blocked by replacing bath Cl- with methanesulfonate.

20 ss sensitive to the DNA damage agent, methyl methanesulfonate.

21 e monofunctional DNA alkylating agent methyl methanesulfonate.

22 yuridine, ethyl methanesulfonate, and methyl methanesulfonate.

23 o sensitive to the DNA-damaging agent methyl methanesulfonate.

24 slightly more sensitive to killing by methyl methanesulfonate.

25 ed exposure at high concentrations of methyl methanesulfonate.

26 han by the general DNA-damaging agent methyl methanesulfonate.

27 lls treated with the alkylating agent methyl methanesulfonate.

28 t their probability to be alkylated by ethyl methanesulfonate.

29 he response to the DNA-damaging agent methyl methanesulfonate.

30 with rapamycin, hydrogen peroxide or methyl methanesulfonate.

31 1-pyrrolidinyl)-cyclohexyl]benzeneacetam ide methanesulfonate (1 microm).

32 en (1s,3s)-3-(tert-butyl)-1-methylcyclobutyl methanesulfonate, 7, reacts in trifluoroethanol is one o

33 After treatment with methyl methanesulfonate, AAG knockdown HeLa cells were delayed

34 maging agents (ultraviolet radiation, methyl methanesulfonate, adriamycin, camptothecin, and cis-Plat

35 Gadd45 protein induction by methyl methanesulfonate also lagged behind JNK activation.

36 romosomal recombination events against ethyl methanesulfonate and acridine mutagen agents.

37 085 GFP-tagged strains in response to methyl methanesulfonate and analyzed 576 GFP strains in five ad

38 itive to DNA-damaging agents, such as methyl methanesulfonate and camptothecin, suggesting a possible

39 ors that elicit DNA damage, including methyl methanesulfonate and ciprofloxacin, as well as those tha

40 ly complement the sensitivity to both methyl methanesulfonate and excess Rad51 in rdh54 null cells.

41 t with DNA damaging agents, including methyl methanesulfonate and gamma-irradiation.

42 hanesulfonate, and with elp3Delta for methyl methanesulfonate and growth at 16 degrees C.

43 icient Escherichia coli cells against methyl methanesulfonate and hydrogen peroxide (H2O2) damage.

44 nsitivity to genotoxic agents such as methyl methanesulfonate and hydroxyurea (HU).

45 the hypersensitivity of sgs1 cells to methyl methanesulfonate and hydroxyurea.

46 o the monofunctional alkylating agent methyl methanesulfonate and leads to further impairment in the

47 methyl-N'nitro-N-nitrosoguanidine and methyl methanesulfonate and longer chain alkylating agents incl

48 fork stalling and collapse caused by methyl methanesulfonate and mitomycin C exposure, a delayed and

49 V light or the radiomimetic chemicals methyl methanesulfonate and mitomycin C.

50 (TOP1) conferred hypersensitivity to methyl methanesulfonate and other DNA-damaging agents, whereas

51 is fen1-1 mutant is hypersensitive to methyl methanesulfonate and shows reduced telomere length.

52 Use of ethyl methanesulfonate and site-directed mutagenesis has ident

53 Using a combination of both ethyl methanesulfonate and site-directed mutagenesis, we have

54 ations of N7-guanine DNA adducts with methyl methanesulfonate and styrene oxide increased with incuba

55 damage caused by the alkylating agent methyl methanesulfonate and that the resulting degradation was

56 DNA-alkylating agents such as ethyl methanesulfonate and the chemotherapeutic drug melphalan

57 n sarcoma HT1080 cells were exposed to ethyl methanesulfonate and Thymitaq selection.

58 nd that knock out of the endonuclease METHYL METHANESULFONATE AND UV SENSITIVE PROTEIN 81 (MUS81) res

59 In both methyl methanesulfonate and UV survival experiments the recA ho

60 fate, nitrate, nitrite, chlorate, sulfamate, methanesulfonate, and fluoride, which can be simultaneou

61 owly, is sensitive to hydroxyurea and methyl methanesulfonate, and is a strong base substitution and

62 let irradiation, 5-fluorodeoxyuridine, ethyl methanesulfonate, and methyl methanesulfonate.

63 for fibroblasts exposed to paraquat, methyl methanesulfonate, and rotenone (P<0.05 in each case for

64 ty to genotoxic stress induced by UV, methyl methanesulfonate, and the replication inhibitor hydroxyu

65 nfers sensitivity to PARP inhibitors, methyl-methanesulfonate, and uracil misincorporation, which ref

66 moderately sensitive to mitomycin C, methyl methanesulfonate, and UV and gamma-radiation, indicating

67 ta for sensitivity to hydroxyurea and methyl methanesulfonate, and with elp3Delta for methyl methanes

68 pecify C(4) leaf anatomy, we generated ethyl methanesulfonate- and gamma-ray-mutagenized populations

69 xyl-2,2,5,5-tetramethyl-3-pyrroline-3-methyl)methanesulfonate] and the denaturant dependences of the

70 s absence, while rates of interconversion of methanesulfonate anomers were determined by NMR exchange

71 fter exposure to the alkylating agent methyl methanesulfonate, approximately 325 gene transcript leve

72 DNA binding mutants are sensitive to methyl methanesulfonate, are not chromatin enriched, and exhibi

73 th acetonitrile, sodium chloride, and sodium methanesulfonate as the sole byproducts.

74 damage and increased cytotoxicity to methyl methanesulfonate as well as increased apoptosis levels w

75 DNA-damaging agents camptothecin and methyl methanesulfonate, as well as hydroxyurea but not to UV l

76 val after DNA damage caused by UV and methyl methanesulfonate, as well as increased genome instabilit

77 54 mutants do not show sensitivity to methyl methanesulfonate at concentrations that sensitize a rad5

78 In recordings obtained with methanesulfonate-based internal solutions, we found an m

79 a and potentiates the cytotoxicity of methyl methanesulfonate between 2- and 5-fold.

80 growth by DNA-damaging agents such as methyl methanesulfonate, bleomycin, camptothecin, and hydroxyur

81 re to either ultraviolet radiation or methyl methanesulfonate but are still able to undergo G2 arrest

82 -dependent clastogens hydroxyurea and methyl methanesulfonate but, as previously observed for D56N an

83 extract from M. methylovora cells grown with methanesulfonate, but not with extract from cells grown

84 zing radiation (IR), cis-platinum and methyl methanesulfonate, but only slight UV radiation sensitivi

85 certain chemical agents (for example methyl methanesulfonate) can induce nucleotide bases on chromos

86 Colistin methanesulfonate (CMS) is the only prodrug of colistin a

87 ministered as the inactive prodrug, colistin methanesulfonate (CMS).

88 onger antimutagenic properties against ethyl methanesulfonate compared to the acridine mutagen agent.

89 aihfA and DeltaihfB strains to UV and methyl methanesulfonate could be complemented with the wild-typ

90 tal toxicants such as methyl mercury, methyl methanesulfonate, crocodilite asbestos or the agents tha

91 ffected in tomato RNA interference and ethyl methanesulfonate-cus1 mutants.

92 -bis(2-chloroethyl)-1-nitrosourea and methyl methanesulfonate cytotoxicity either when these agents w

93 lity of these compounds to potentiate methyl methanesulfonate cytotoxicity, an indicator of cellular

94 DNA replication but is important for methyl methanesulfonate damage-induced DNA repair.

95 Interestingly, this ethyl methanesulfonate-derived mutant shows unusual chromosoma

96 The ethyl methanesulfonate-derived vte3-1 allele alters tocopherol

97 ontrast to previous in vitro results, methyl methanesulfonate did not induce stress-activated signal

98 ic compounds 4-nitroquinoline N-oxide, ethyl methanesulfonate, diethylstilbestrol, and 2-aminoanthrac

99 ioleyl-3,3,3',3'-tetramethylindocarbocyanine methanesulfonate (DiI) into the dorsal motor nucleus of

100 oleyl-3,3,3;, 3;-tetramethylindocarbocyanine methanesulfonate (DiI) into the nucleus ambiguus (NA) an

101 l-3, 3, 3'', 3''-tetramethylindocarbocyanine methanesulfonate (DiI) was performed at day 36 after TBI

102 The methanesulfonate donors are prepared in situ from glycos

103 on of ribosomal proteins depending on methyl methanesulfonate dose was shown to correlate with cell g

104 The ionic liquid 1-ethyl-3-methylimidazolium methanesulfonate ([EMIM][MeSO(3)]) has been considered a

105 fied SAFEGUARD1 (SAFE1) in a screen of ethyl methanesulfonate (EMS) mutagenized flu ex1 plants for su

106 sformed luciferase reporter lines were ethyl methanesulfonate (EMS) mutagenized, and stable M(2) seed

107 Here, we identified one ethyl methanesulfonate (EMS) mutant, deeply serrated (des), in

108 Two N. benthamiana ethyl methanesulfonate (EMS) mutants deficient for XopJ4 perce

109 Ethyl methanesulfonate (EMS) mutants of tomato have already pr

110 xamine Scp160p function, we applied an ethyl methanesulfonate (EMS) screen for loci synthetically let

111 ing for autosomes heavily treated with ethyl methanesulfonate (EMS), approximately 12,000 lines in wh

112 tment with either 1 mM octanol, 0.5 mM ethyl methanesulfonate (EMS), or cytoplasmic acidification, wi

113 mes) method combines the efficiency of ethyl methanesulfonate (EMS)-induced mutagenesis with the abil

114 hensive analysis of approximately 1900 ethyl methanesulfonate (EMS)-induced mutations in 192 Arabidop

115 r a specific phenotype, observed in an ethyl methanesulfonate (EMS)-mutagenized Caenorhabditis elegan

116 n is evident in more than one-third of ethyl methanesulfonate (EMS)-treated bal M(1) plants.

117 er males by treating them with 21.2 mm ethyl methanesulfonate (EMS).

118 e of a diarylborinic acid catalyst, glycosyl methanesulfonates engage in regio- and stereoselective c

119 ious role of water during the formation of a methanesulfonate ester in the 1-pot activation/displacem

120 nternally applied 2-(trimethylammonium)ethyl methanesulfonate failed to cause desensitization (despit

121 psis (Arabidopsis thaliana), including ethyl methanesulfonate, fast-neutron and defined T-DNA mutants

122 V light (generating UV photoproducts), ethyl methanesulfonate (generating alkylation damage), mitomyc

123 After mutagenesis with ethyl methanesulfonate, growing cells were selectively killed

124 t elution strength was found to be acetate > methanesulfonate > trifluoroacetate > perchlorate.

125 thylsulfonyl-4-piperidino-benzoyl)-guanidine methanesulfonate (HOE 694) in HEPES buffer.

126 1-pyrrolidinyl)-cyclohexyl] benzeneacetamide methanesulfonate hydrate was preserved despite the absen

127 of JNK/p38 activities in response to methyl methanesulfonate, hydrogen peroxide, UVC irradiation, so

128 brought about by treatments with UV, methyl methanesulfonate, hydroxyurea, and aphidicolin.

129 N3-methyladenine nor the toxicity of methyl methanesulfonate in E. coli.

130 ivity of dap1Delta to fluconazole and methyl methanesulfonate in S. cerevisiae.

131 sensitivity to the DNA-damaging agent methyl methanesulfonate in the absence of any additional mutati

132 (dpms)Pd(II)Me(OH2) (8) (dpms = di(2-pyridyl)methanesulfonate) in water in the pH range of 6-14 at 21

133 ure lethality and hypersensitivity to methyl methanesulfonate, in a manner corresponding to the in vi

134 pms)Pt(II)Me(OH)(-) (2) [dpms = di(2-pyridyl)methanesulfonate] in water in the pH range of 4-14 at 21

135 f CAF-I- or RCAF-defective cells with methyl methanesulfonate increased the induction of GCRs compare

136 ssion spectrum obtained for trimethylaminium methanesulfonate, indicating the formation of the salt o

137 cid-induced double-strand breaks, and methyl methanesulfonate-induced alkylation and that RecB and Re

138 ity of beta-pol-deficient cells after methyl methanesulfonate-induced alkylation damage is wholly dep

139 on, we identified three closely linked ethyl methanesulfonate-induced changes as putative candidates.

140 displayed attenuated DNA repair after methyl methanesulfonate-induced damage compared with E2F1(+/+)

141 g wild-type, but not mutant E2F1, and methyl methanesulfonate-induced DNA damage stimulated XRCC1 exp

142 s2 synergistically sensitize cells to methyl methanesulfonate-induced DNA damage.

143 the efficient repair of nonclustered methyl methanesulfonate-induced lesions, as measured by quantit

144 in the extent to which they promoted methyl methanesulfonate-induced mutagenesis.

145 In the ethyl methanesulfonate-induced mutant hcf222-1, the accumulati

146 ts in rarity of such mutants, with the ethyl methanesulfonate-induced mutant ms5 among the few report

147 ysis of a previously identified tomato ethyl methanesulfonate-induced mutant that exhibits abnormal m

148 sensitive to salt stress (hss) from an ethyl methanesulfonate-induced mutation population.

149 equency and spectra of spontaneous and ethyl methanesulfonate-induced mutations across the Saccharomy

150 Moreover, ethyl methanesulfonate-induced mutations that change amino aci

151 Ethyl methanesulfonate-induced mutations within the second B-b

152 Neither function is affected in ethyl-methanesulfonate-induced Pl1-Rhoades derivatives that pr

153 We conducted a screen for ethyl methanesulfonate-induced suppressors of Arabidopsis thal

154 2-(pyrrolidinyl)cyclohexyl] benzeneacetamide methanesulfonate), inhibited adenosine diphosphate (ADP)

155 ctadecyl-3,3,3',3-tetramethlindocarbocyanine methanesulfonate) injected into multiple sites in the wa

156 A second pathway may use a methanesulfonate intermediate to convert methionine-deri

157 lele (sob3-4) was generated through an ethyl methanesulfonate intragenic suppressor screen of sob3-D

158 picoseconds and results in the formation of methanesulfonate ion (MSA(-))H3O(+) ion pair.

159 -(4-nitrobenzyloxy)phenyl)ethyl)-isothiourea methanesulfonate (KB-R7943) and the structurally related

160 ng the cells to either hydroxyurea or methyl methanesulfonate, lending support for a DDK role in stab

161 cell death and were unable to repair methyl methanesulfonate lesions.

162 r Cl(-) with the impermeable and inert anion methanesulfonate (MeSO(3)(-)) caused ASIC1a currents to

163 tress induced by hydroxyurea (HU) and methyl methanesulfonate (MMS) activates DNA integrity checkpoin

164 re found to be hypersensitive to both methyl methanesulfonate (MMS) and 5-hydroxymethyl-2'-deoxyuridi

165 ive to DNA-damaging reagents, such as methyl methanesulfonate (MMS) and H2O2.

166 n response to the DNA-damaging agents methyl methanesulfonate (MMS) and hydroxyurea by a mechanism(s)

167 s to the survival of cells exposed to methyl methanesulfonate (MMS) and in the absence of Mag1, Rad30

168 roblasts, to the cytotoxic effects of methyl methanesulfonate (MMS) and methylnitrosourea.

169 ance to DNA damaging reagents such as methyl methanesulfonate (MMS) and N-methyl-N-nitrosourea (MNU),

170 rom C. Zuker) for hypersensitivity to methyl methanesulfonate (MMS) and nitrogen mustard (HN2).

171 rred a similar level of resistance to methyl methanesulfonate (MMS) and temozolomide (TMZ) but simult

172 tel1-Delta that cause sensitivity to methyl methanesulfonate (MMS) and/or ionizing radiation, along

173 d sensitivity to the alkylating agent methyl methanesulfonate (MMS) compared to the parent strain.

174 c responses to the DNA damaging agent methyl methanesulfonate (MMS) in comparison to responses to acu

175 notoxic agents ionizing radiation and methyl methanesulfonate (MMS) in predominantly p53 wild-type ce

176 ER in vivo, we examined the repair of methyl methanesulfonate (MMS) induced DNA damage in haploid G1

177 e, resistance to the alkylating agent methyl methanesulfonate (MMS) is mediated in part by Dap1p (dam

178 r, we find that DNA damages caused by methyl methanesulfonate (MMS) or etoposide promote the formatio

179 presence of the DNA alkylating agent methyl methanesulfonate (MMS) over 50% of clb5 clb6 mutants by-

180 iles for 3AT and the alkylating agent methyl methanesulfonate (MMS) overlapped extensively, and MMS i

181 t on mutation, recombination, and the methyl methanesulfonate (MMS) response in repair-competent cell

182 Two subtle cac3 phenotypes, slight methyl methanesulfonate (MMS) sensitivity and reduction of telo

183 suppressed the camptothecin (CPT) and methyl methanesulfonate (MMS) sensitivity of nuclease-deficient

184 ct on a larval mitotic checkpoint and methyl methanesulfonate (MMS) sensitivity.

185 osylase (AAG), along with exposure to methyl methanesulfonate (MMS) to study mutagenesis as a functio

186 phase in response to hydroxy urea or methyl methanesulfonate (MMS) treatment.

187 A2 were shown to be hypersensitive to methyl methanesulfonate (MMS) treatment.

188 d sensitivity to the alkylating agent methyl methanesulfonate (MMS) was also observed for siRNA-media

189 t, to investigate this question using methyl methanesulfonate (MMS), a base-damaging agent.

190 f the three major gadd transcripts by methyl methanesulfonate (MMS), and almost completely blocks the

191 rad30 mutant cells were sensitive to methyl methanesulfonate (MMS), and rev1 rad30 or rev3 rad30 dou

192 mined the mutation spectrum caused by methyl methanesulfonate (MMS), and showed that MMS also induces

193 , sensitivity to hydroxyurea (HU) and methyl methanesulfonate (MMS), and ubiquitination of proliferat

194 resistance to the DNA-damaging agent methyl methanesulfonate (MMS), as determined by chemogenomic fi

195 reatment with UV, mitomycin C (MC) or methyl methanesulfonate (MMS), as well as homologous recombinat

196 hypersensitive to the genotoxic agent methyl methanesulfonate (MMS), but the molecular basis of genot

197 Alkylating agents, such as methyl methanesulfonate (MMS), damage DNA and activate the DNA

198 ys, ultraviolet (UV)-C radiation, and methyl methanesulfonate (MMS), indicating the broad relevance o

199 hanism by which a DNA damaging agent, methyl methanesulfonate (MMS), induces RTP801 transcription.

200 ing agents, including UV irradiation, methyl methanesulfonate (MMS), mitomycin C, phleomycin, hydroge

201 sure to hydrogen peroxide (H(2)O(2)), methyl methanesulfonate (MMS), or camptothecin by monitoring NA

202 4-nitroquinoline 1-oxide (4-NQO) and methyl methanesulfonate (MMS), or when an HO endonuclease-induc

203 he presence of the DNA-damaging agent methyl methanesulfonate (MMS), TOR-dependent cell survival requ

204 In contrast, GADD45 induction by methyl methanesulfonate (MMS), UV radiation (UV), and medium st

205 e treated with the DNA-damaging agent methyl methanesulfonate (MMS), we carried out two-dimensional g

206 e progression of replication forks in methyl-methanesulfonate (MMS)-damaged cells, under different co

207 ever, we found that in vivo repair of methyl methanesulfonate (MMS)-induced alkylation damage in DNA

208 Ionizing radiation and methyl methanesulfonate (MMS)-induced DNA damage did not exhibi

209 ting H2B K111 impairs the response to methyl methanesulfonate (MMS)-induced DNA lesions and disrupts

210 gating enzyme UBC13 (E2) and promotes methyl methanesulfonate (MMS)-induced PCNA polyubiquitination.

211 lls treated with the alkylating agent methyl methanesulfonate (MMS).

212 the toxicity of the alkylating agent methyl methanesulfonate (MMS).

213 ly after treatment with the genotoxin methyl methanesulfonate (MMS).

214 tors (TFs) after exposure of yeast to methyl-methanesulfonate (MMS).

215 tive to ultraviolet (UV) light and to methyl methanesulfonate (MMS).

216 tional DNA methylating agents such as methyl methanesulfonate (MMS).

217 background results in sensitivity to methyl methanesulfonate (MMS).

218 A-damaging alkylating agents, such as methyl methanesulfonate (MMS).

219 n treatment with the alkylating agent methyl methanesulfonate (MMS).

220 ast treated with the alkylating agent methyl methanesulfonate (MMS).

221 fter exposure to the alkylating agent methyl methanesulfonate (MMS).

222 es C but do not affect sensitivity to methyl methanesulfonate (MMS).

223 wide screen for sensitivity to 0.001% methyl methanesulfonate (MMS).

224 g recovery from DNA damage induced by methyl methanesulfonate (MMS).

225 cells, with and without DNA damage by methyl methanesulfonate (MMS).

226 n on exposure to the alkylating agent methyl methanesulfonate (MMS).

227 retrogradely labeled with aminostilbamidine methanesulfonate (Molecular Probes, Eugene, OR), and los

228 PvGal biosynthesis was investigated by ethyl methanesulfonate mutagenesis of S. pombe, followed by th

229 Ethyl methanesulfonate mutagenesis of the model legume Medicag

230 trachomatis was subjected to low-level ethyl methanesulfonate mutagenesis to generate chlamydiae that

231 utagenized oat population, produced by ethyl methanesulfonate mutagenesis, hulled grains from 17 line

232 nse umuD' mutants deficient in UV and methyl methanesulfonate mutagenesis.

233 TG01 and TG10, were generated through ethyl methanesulfonate mutagenesis.

234 ined a petal-closed flower mutation by ethyl methanesulfonate mutagenesis.

235 ul symbiotic infection, we screened an ethyl methanesulfonate mutagenized population of Lotus japonic

236 A subset of an ethyl methanesulfonate mutagenized population of soybean (Glyc

237 eny and a half million F(3) progeny of ethyl-methanesulfonate-mutagenized animals were treated in thr

238 um was carried out for a population of ethyl methanesulfonate-mutagenized Arabidopsis (Arabidopsis th

239 We screened 4,960 ethyl methanesulfonate-mutagenized colonies for defects in int

240 (spl11) mutant was identified from an ethyl methanesulfonate-mutagenized indica cultivar IR68 popula

241 we report the identification of eight ethyl methanesulfonate-mutagenized loss-of-function bin2 allel

242 e (vyl) phenotype was identified in an ethyl methanesulfonate-mutagenized population derived from the

243 in seed Fe homeostasis, we screened an ethyl methanesulfonate-mutagenized population of nramp3nramp4

244 By screening ethyl methanesulfonate-mutagenized populations of Arabidopsis,

245 We screened cotyledons from ethyl methanesulfonate-mutagenized seeds of Arabidopsis by lig

246 An ethyl methanesulfonate mutant (jar1) with decreased sensitivit

247 and cuticle in tomato, we screened an ethyl methanesulfonate mutant collection in the miniature toma

248 an Arabidopsis (Arabidopsis thaliana) ethyl methanesulfonate mutant, modified vacuole phenotype1-1 (

249 In parallel, three independent ethyl methanesulfonate mutants in the S. lycopersicum cultivar

250 We have isolated several ethyl methanesulfonate mutants of salt cress that have reduced

251 to 10-fold increase in sensitivity to methyl methanesulfonate, N-methyl-N-nitrosourea, and the chemot

252 gents including N-ethyl-N-nitrosourea, ethyl methanesulfonate, N-propyl-N-nitrosourea and N-butyl-N-n

253 partially rescued the sensitivity to methyl methanesulfonate of Saccharomyces cerevisiae sgs1 mutant

254 and promote resistance to killing by methyl methanesulfonate, one gene (EGL1) previously identified

255 e capacitation, Cl(-) was replaced by either methanesulfonate or gluconate two nonpermeable anions.

256 in isc1Delta cells when treated with methyl methanesulfonate or HU.

257 uitinated when cells are treated with methyl methanesulfonate or hydrogen peroxide.

258 is by GADD34 following treatment with methyl-methanesulfonate or ionizing radiation in HEK293 and HeL

259 ffect on sensitivity to UV radiation, methyl methanesulfonate, or quinolone antibiotics.

260 ituted cysteines to covalent modification by methanesulfonate reagent depends on the agonist site at

261 f wt-NBCe1-A, whose activity is resistant to methanesulfonate reagents, and an NBCe1-A(T442C) mutant,

262 t, whose activity is completely inhibited by methanesulfonate reagents, confirmed that NBCe1-A monome

263 s were dissected from AQP1 currents using Cs-methanesulfonate recording salines; the background curre

264 Furthermore, methyl methanesulfonate reduced NAD(P)H in PARP-1+/+ cells, whe

265 ccurs in p53 wild-type cells, whereas methyl methanesulfonate regulation of KILLER/DR5 occurs in a p5

266 However, treatment with methyl methanesulfonate resulted in three- to fourfold more hpr

267 fects of the KOR agonist (+/-)-trans-U-50488 methanesulfonate salt (U-50488) (.0-10.0 mg/kg) on brain

268 phenyl] methylene]-2-imino-4-thiazolidinone, methanesulfonate salt), was discovered as a dual inhibit

269 novel Pd- and base-promoted rearrangement of methanesulfonate salts of isoxazolidine to bridge bicycl

270 the rdh54 null mutation enhances the methyl methanesulfonate sensitivity of a rad54 mutant and singl

271 DNAs complemented the temperature and methyl methanesulfonate sensitivity of a yeast rad27 deletion,

272 ylatable lysines of H3 for heightened methyl methanesulfonate sensitivity to be observed.

273 utator strains also slightly enhanced methyl methanesulfonate sensitivity.

274 indazol -1-yl)-phenylamino]-cyclohexyl ester methanesulfonate (SNX-5422, 10) was orally bioavailable

275 ellobioside-6,8-difluoro-7-hydroxycoumarin-4-methanesulfonate substrate was used to assay cellobiohyd

276 resistance to the DNA damaging agent methyl methanesulfonate, suggesting this pathway negatively reg

277 comprising the impermeant anions aspartate, methanesulfonate, sulfate, or HEPES.

278 ight into GDU1's role, we searched for ethyl-methanesulfonate suppressor mutants and performed yeast-

279 BZR1) and BRASSINOSTEROID INSENSITIVE1-ETHYL METHANESULFONATE-SUPPRESSOR1 (BES1)/BZR2, blocks these r

280 A BRASSINOSTEROID INSENSITIVE1-ETHYL METHANESULFONATE-SUPPRESSOR1-yellow fluorescent protein

281 polysaccharide were more resistant to methyl methanesulfonate than untreated cells.

282 es of cells to the DNA-damaging agent methyl methanesulfonate, the replication inhibitor hydroxyurea,

283 cloheexadienl-yl) decyl triphenylphosphonium methanesulfonate]) to prevent AD-like pathology in mouse

284 collection of 12,326 strains carrying ethyl-methanesulfonate-treated, homozygous viable second or th

285 g RNA renders HeLa cells sensitive to methyl methanesulfonate treatment by a mechanism of shortened h

286 ponse to DNA damage induced by either methyl methanesulfonate treatment or ionizing radiation, increa

287 an mutant M(krk) survived poorly upon methyl methanesulfonate treatment or when they were incubated a

288 Moreover, during the first 30 min of methyl methanesulfonate treatment, the rise in Gklf mRNA level

289 romosomal breaks and are sensitive to methyl methanesulfonate treatment.

290 counteranion also was investigated (acetate, methanesulfonate, trifluoroacetate, and perchlorate), an

291 uding hexafluorophosphate, acetate, nitrate, methanesulfonate, trifluoroacetate, and trifluoromethyls

292 1-pyrrolidinyl]cyclohexyl) benzene-acetamide methanesulfonate (U-50,488H; 1 microM), and baclofen (50

293 2-(1-pyrolidinyl)cyclohexyl] benzeneaceamide methanesulfonate (U50,488H).

294 In response to DNA damage induced by methyl methanesulfonate, USP11 could counteract RNF4 to inhibit

295 4-(4-nitrobenzyloxy)phenyl]ethyl]isothiourea methanesulfonate) was reported to selectively inhibit th

296 e and luteolin-7-O-glucuronide against ethyl methanesulfonate were 57.6%, 58.3% and 62.5%, respective

297 ypersensitive to the alkylating agent methyl methanesulfonate, which creates DNA damage that is prima

298 For methyl methanesulfonate, which does not sequence selectively me

299 yzed metalation of (R)- and (S)-3-butyn-2-ol methanesulfonate with Et(2)Zn and InI.

300 S(N)2 displacements of the corresponding methanesulfonates with pyrophosphate and methanediphosph