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 han by the general DNA-damaging agent methyl methanesulfonate.

5 uced by camptothecin, hydroxyurea and methyl-methanesulfonate.

6 sitivity to the DNA-methylating agent methyl methanesulfonate.

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

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

9 e breast cancer cells' sensitivity to methyl methanesulfonate.

10 XRCC1-deficient CHO cells exposed to methyl methanesulfonate.

11 nd in HAT1 resulted in sensitivity to methyl methanesulfonate.

12 n was prepared by mutagenesis by using ethyl methanesulfonate.

13 bleomycin but not to damage caused by methyl methanesulfonate.

14 p53 expression in cells treated with methyl methanesulfonate.

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

16 sensitivity to the DNA-damaging agent methyl methanesulfonate.

17 MO was specifically induced during growth on methanesulfonate.

18 eprivation and DNA damage elicited by methyl methanesulfonate.

19 li to killing by the alkylating agent methyl methanesulfonate.

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

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

22 e monofunctional DNA alkylating agent methyl methanesulfonate.

23 yuridine, ethyl methanesulfonate, and methyl methanesulfonate.

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

25 slightly more sensitive to killing by methyl methanesulfonate.

26 ed exposure at high concentrations of methyl methanesulfonate.

27 (1-pyrrolidinyl)cyclohexyl]ben zeneacetamide methanesulfonate.

28 visiae, the cells became sensitive to methyl methanesulfonate.

29 lls treated with the alkylating agent methyl methanesulfonate.

30 t their probability to be alkylated by ethyl methanesulfonate.

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

32 with rapamycin, hydrogen peroxide or methyl methanesulfonate.

33 1-pyrrolidinyl)-cyclohexyl]benzeneacetam ide methanesulfonate (1 microm).

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

35 ne, UV light, ionizing radiation, and methyl methanesulfonate activate p38 MAP kinase.

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

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

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

39 085 GFP-tagged strains in response to methyl methanesulfonate and analyzed 576 GFP strains in five ad

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

75 54 mutants do not show sensitivity to methyl methanesulfonate at concentrations that sensitize a rad5

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

98 ioleyl-3,3,3',3'-tetramethylindocarbocyanine methanesulfonate (DiI) into the nodose ganglia of animal

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

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

101 The methanesulfonate donors are prepared in situ from glycos

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

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

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

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

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

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

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

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

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

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

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

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

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

115 nogen x-rays, ethyl methanesulfonate, methyl methanesulfonate, ethyl nitrosourea, benzo[a]pyrene, tri

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

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

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

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

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

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

122 1-pyrrolidinyl)-cyclohexyl] benzeneacetamide methanesulfonate hydrate was preserved despite the absen

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

147 2-(pyrrolidinyl)cyclohexyl] benzeneacetamide methanesulfonate), inhibited adenosine diphosphate (ADP)

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

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

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

151 In cells treated with ethyl methanesulfonate, intragenic deletions were detected in

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

153 -(4-nitrobenzyloxy)phenyl)ethyl)-isothiourea methanesulfonate (KB-R7943) and the structurally related

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

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

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

157 re inducible by the carcinogen x-rays, ethyl methanesulfonate, methyl methanesulfonate, ethyl nitroso

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

173 I or the DNA-damaging chemical agents methyl methanesulfonate (MMS) or 4-nitroquinoline 1-oxide (4-NQ

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

196 NA include alkylating agents, such as methyl methanesulfonate (MMS), N-methyl-N'-nitro-N-nitrosoguani

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

198 4-nitroquinoline 1-oxide (4-NQO) and methyl methanesulfonate (MMS), or when an HO endonuclease-induc

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

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

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

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

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

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

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

206 dd153 in all the c-myc transfectants, methyl methanesulfonate (MMS)-induced transcription of the gadd

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

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

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

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

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

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

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

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

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

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

217 nt of cells with the alkylating agent methyl methanesulfonate (MMS).

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

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

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

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

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

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

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

225 Ethyl methanesulfonate mutagenesis of the model legume Medicag

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

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

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

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

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

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

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

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

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

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

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

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

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

239 By screening ethyl methanesulfonate-mutagenized populations of Arabidopsis,

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

241 An ethyl methanesulfonate mutant (jar1) with decreased sensitivit

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

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

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

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

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

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

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

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

250 xanthus dsp were mutagenized either by ethyl methanesulfonate or by Tn5 insertions.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

266 ression of the mouse cDNA rescued the methyl methanesulfonate-sensitive phenotype in rad50 mutant yea

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

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

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

270 utant alleles exhibited higher UV and methyl methanesulfonate sensitivity, increased rates of spontan

271 utator strains also slightly enhanced methyl methanesulfonate sensitivity.

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

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

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

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

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

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

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

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

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

281 tion properties, were mutagenized with ethyl methanesulfonate to obtain variants that were induced (i

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

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

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

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

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

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

288 romosomal breaks and are sensitive to methyl methanesulfonate treatment.

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

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

291 1-pyrrolidinyl]cyclohexyl) benzene-acetamide methanesulfonate (U-50,488H; 1 microM), and baclofen (50

292 2-(1-pyrolidinyl)cyclohexyl] benzeneaceamide methanesulfonate (U50,488H).

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

294 ity of UV40 to mitomycin C, cisplatin, ethyl methanesulfonate, UV, and gamma-radiation.

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