ライフサイエンスコーパス: methyl methanesulfonate

1 reated with the DNA-damaging agents H2O2 and methyl methanesulfonate.

2 reatment with the DNA-damaging agents UV and methyl methanesulfonate.

3 ased the breast cancer cells' sensitivity to methyl methanesulfonate.

4 (P)H in XRCC1-deficient CHO cells exposed to methyl methanesulfonate.

5 tail and in HAT1 resulted in sensitivity to methyl methanesulfonate.

6 tress than by the general DNA-damaging agent methyl methanesulfonate.

7 O2 and bleomycin but not to damage caused by methyl methanesulfonate.

8 ld-type p53 expression in cells treated with methyl methanesulfonate.

9 their sensitivity to the DNA-damaging agent methyl methanesulfonate.

10 serum deprivation and DNA damage elicited by methyl methanesulfonate.

11 d E. coli to killing by the alkylating agent methyl methanesulfonate.

12 them less sensitive to the DNA damage agent, methyl methanesulfonate.

13 e to the monofunctional DNA alkylating agent methyl methanesulfonate.

14 orodeoxyuridine, ethyl methanesulfonate, and methyl methanesulfonate.

15 are also sensitive to the DNA-damaging agent methyl methanesulfonate.

16 nt and slightly more sensitive to killing by methyl methanesulfonate.

17 prolonged exposure at high concentrations of methyl methanesulfonate.

18 es cerevisiae, the cells became sensitive to methyl methanesulfonate.

19 sylcytosine but not after exposure to UV and methyl methanesulfonate.

20 ty to killing by UV or gamma radiation or to methyl methanesulfonate.

21 id-treated DNA and in human cells exposed to methyl methanesulfonate.

22 tant cells treated with the alkylating agent methyl methanesulfonate.

23 y for the response to the DNA-damaging agent methyl methanesulfonate.

24 eatment with rapamycin, hydrogen peroxide or methyl methanesulfonate.

25 on and sensitivity to the DNA-damaging agent methyl methanesulfonate.

26 cerevisiae treated with the alkylating agent methyl methanesulfonate.

27 sensitive to treatment with mitomycin C and methyl methanesulfonate.

28 ypersensitivity to the DNA-methylating agent methyl methanesulfonate.

29 age induced by camptothecin, hydroxyurea and methyl-methanesulfonate.

30 After treatment with methyl methanesulfonate, AAG knockdown HeLa cells were d

31 lcytosine, UV light, ionizing radiation, and methyl methanesulfonate activate p38 MAP kinase.

32 DNA-damaging agents (ultraviolet radiation, methyl methanesulfonate, adriamycin, camptothecin, and c

33 Gadd45 protein induction by methyl methanesulfonate also lagged behind JNK activatio

34 ted in BiP-overexpressing cells treated with methyl methanesulfonate, an agent thought to activate CH

35 s in 4,085 GFP-tagged strains in response to methyl methanesulfonate and analyzed 576 GFP strains in

36 persensitive to DNA-damaging agents, such as methyl methanesulfonate and camptothecin, suggesting a p

37 stressors that elicit DNA damage, including methyl methanesulfonate and ciprofloxacin, as well as th

38 fectively complement the sensitivity to both methyl methanesulfonate and excess Rad51 in rdh54 null c

39 reatment with DNA damaging agents, including methyl methanesulfonate and gamma-irradiation.

40 hyl methanesulfonate, and with elp3Delta for methyl methanesulfonate and growth at 16 degrees C.

41 ase-deficient Escherichia coli cells against methyl methanesulfonate and hydrogen peroxide (H2O2) dam

42 ibit sensitivity to genotoxic agents such as methyl methanesulfonate and hydroxyurea (HU).

43 luding the hypersensitivity of sgs1 cells to methyl methanesulfonate and hydroxyurea.

44 ivity to the monofunctional alkylating agent methyl methanesulfonate and leads to further impairment

45 rea, N-methyl-N'nitro-N-nitrosoguanidine and methyl methanesulfonate and longer chain alkylating agen

46 ication fork stalling and collapse caused by methyl methanesulfonate and mitomycin C exposure, a dela

47 ls to UV light or the radiomimetic chemicals methyl methanesulfonate and mitomycin C.

48 erase I (TOP1) conferred hypersensitivity to methyl methanesulfonate and other DNA-damaging agents, w

49 abidopsis fen1-1 mutant is hypersensitive to methyl methanesulfonate and shows reduced telomere lengt

50 oncentrations of N7-guanine DNA adducts with methyl methanesulfonate and styrene oxide increased with

51 on DNA damage caused by the alkylating agent methyl methanesulfonate and that the resulting degradati

52 itivity of the parasite to both the mutagen, methyl methanesulfonate and the antimalarial drug dihydr

53 we found that knock out of the endonuclease METHYL METHANESULFONATE AND UV SENSITIVE PROTEIN 81 (MUS

54 In both methyl methanesulfonate and UV survival experiments the

55 ith mutations in a second ICL repair factor, METHYL METHANESULFONATE AND UV-SENSITIVE PROTEIN 81 (MUS

56 The nuclease METHYL METHANESULFONATE AND UV-SENSITIVE PROTEIN 81 (MUS

57 rows slowly, is sensitive to hydroxyurea and methyl methanesulfonate, and is a strong base substituti

58 bserved for fibroblasts exposed to paraquat, methyl methanesulfonate, and rotenone (P<0.05 in each ca

59 nsitivity to genotoxic stress induced by UV, methyl methanesulfonate, and the replication inhibitor h

60 re also moderately sensitive to mitomycin C, methyl methanesulfonate, and UV and gamma-radiation, ind

61 dph1Delta for sensitivity to hydroxyurea and methyl methanesulfonate, and with elp3Delta for methyl m

62 ALC1 confers sensitivity to PARP inhibitors, methyl-methanesulfonate, and uracil misincorporation, wh

63 L [(1-oxyl-2,2,5,5-tetramethyl-3-pyrroline-3-methyl)methanesulfonate] and the denaturant dependences

64 that, after exposure to the alkylating agent methyl methanesulfonate, approximately 325 gene transcri

65 complex DNA binding mutants are sensitive to methyl methanesulfonate, are not chromatin enriched, and

66 in DNA damage and increased cytotoxicity to methyl methanesulfonate as well as increased apoptosis l

67 to the DNA-damaging agents camptothecin and methyl methanesulfonate, as well as hydroxyurea but not

68 d survival after DNA damage caused by UV and methyl methanesulfonate, as well as increased genome ins

69 but rdh54 mutants do not show sensitivity to methyl methanesulfonate at concentrations that sensitize

70 than 3a and potentiates the cytotoxicity of methyl methanesulfonate between 2- and 5-fold.

71 ion of growth by DNA-damaging agents such as methyl methanesulfonate, bleomycin, camptothecin, and hy

72 exposure to either ultraviolet radiation or methyl methanesulfonate but are still able to undergo G2

73 S-phase-dependent clastogens hydroxyurea and methyl methanesulfonate but, as previously observed for

74 to ionizing radiation (IR), cis-platinum and methyl methanesulfonate, but only slight UV radiation se

75 tes and certain chemical agents (for example methyl methanesulfonate) can induce nucleotide bases on

76 oplatin, bleomycin, camptothecin, etoposide, methyl methanesulfonate, cisplatin, mitomycin C, and Tax

77 to CATR1.3 isolated from tumors produced by methyl methanesulfonate-converted, nontransplantable hum

78 li DeltaihfA and DeltaihfB strains to UV and methyl methanesulfonate could be complemented with the w

79 ironmental toxicants such as methyl mercury, methyl methanesulfonate, crocodilite asbestos or the age

80 nst 1,3-bis(2-chloroethyl)-1-nitrosourea and methyl methanesulfonate cytotoxicity either when these a

81 The ability of these compounds to potentiate methyl methanesulfonate cytotoxicity, an indicator of ce

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

83 e, in contrast to previous in vitro results, methyl methanesulfonate did not induce stress-activated

84 odulation of ribosomal proteins depending on methyl methanesulfonate dose was shown to correlate with

85 e carcinogen x-rays, ethyl methanesulfonate, methyl methanesulfonate, ethyl nitrosourea, benzo[a]pyre

86 teractions primarily with a single compound (methyl methanesulfonate for RNF25) or a set of related c

87 parison of JNK/p38 activities in response to methyl methanesulfonate, hydrogen peroxide, UVC irradiat

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

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

90 otoxic synergism with the DNA damaging agent methyl methanesulfonate in HeLa cells.

91 sensitivity of dap1Delta to fluconazole and methyl methanesulfonate in S. cerevisiae.

92 reased sensitivity to the DNA-damaging agent methyl methanesulfonate in the absence of any additional

93 emperature lethality and hypersensitivity to methyl methanesulfonate, in a manner corresponding to th

94 tment of CAF-I- or RCAF-defective cells with methyl methanesulfonate increased the induction of GCRs

95 dixic acid-induced double-strand breaks, and methyl methanesulfonate-induced alkylation and that RecB

96 ensitivity of beta-pol-deficient cells after methyl methanesulfonate-induced alkylation damage is who

97 enders cells significantly more sensitive to methyl methanesulfonate-induced chromosome damage, and t

98 ) MEFs displayed attenuated DNA repair after methyl methanesulfonate-induced damage compared with E2F

99 pressing wild-type, but not mutant E2F1, and methyl methanesulfonate-induced DNA damage stimulated XR

100 and srs2 synergistically sensitize cells to methyl methanesulfonate-induced DNA damage.

101 ts with the efficient repair of nonclustered methyl methanesulfonate-induced lesions, as measured by

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

103 exposing the cells to either hydroxyurea or methyl methanesulfonate, lending support for a DDK role

104 est and cell death and were unable to repair methyl methanesulfonate lesions.

105 ation stress induced by hydroxyurea (HU) and methyl methanesulfonate (MMS) activates DNA integrity ch

106 CSB were found to be hypersensitive to both methyl methanesulfonate (MMS) and 5-hydroxymethyl-2'-deo

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

108 lated in response to the DNA-damaging agents methyl methanesulfonate (MMS) and hydroxyurea by a mecha

109 tributes to the survival of cells exposed to methyl methanesulfonate (MMS) and in the absence of Mag1

110 nic fibroblasts, to the cytotoxic effects of methyl methanesulfonate (MMS) and methylnitrosourea.

111 resistance to DNA damaging reagents such as methyl methanesulfonate (MMS) and N-methyl-N-nitrosourea

112 ained from C. Zuker) for hypersensitivity to methyl methanesulfonate (MMS) and nitrogen mustard (HN2)

113 o conferred a similar level of resistance to methyl methanesulfonate (MMS) and temozolomide (TMZ) but

114 ns with tel1-Delta that cause sensitivity to methyl methanesulfonate (MMS) and/or ionizing radiation,

115 ncreased sensitivity to the alkylating agent methyl methanesulfonate (MMS) compared to the parent str

116 any sensitivity to ionizing radiation or to methyl methanesulfonate (MMS) conferred by a hdf1 deleti

117 genomic responses to the DNA damaging agent methyl methanesulfonate (MMS) in comparison to responses

118 the genotoxic agents ionizing radiation and methyl methanesulfonate (MMS) in predominantly p53 wild-

119 igate BER in vivo, we examined the repair of methyl methanesulfonate (MMS) induced DNA damage in hapl

120 revisiae, resistance to the alkylating agent methyl methanesulfonate (MMS) is mediated in part by Dap

121 e Pvu II or the DNA-damaging chemical agents methyl methanesulfonate (MMS) or 4-nitroquinoline 1-oxid

122 Moreover, we find that DNA damages caused by methyl methanesulfonate (MMS) or etoposide promote the f

123 mically induced DNA replication stress using methyl methanesulfonate (MMS) or hydroxyurea (HU).

124 in the presence of the DNA alkylating agent methyl methanesulfonate (MMS) over 50% of clb5 clb6 muta

125 on profiles for 3AT and the alkylating agent methyl methanesulfonate (MMS) overlapped extensively, an

126 e effect on mutation, recombination, and the methyl methanesulfonate (MMS) response in repair-compete

127 Two subtle cac3 phenotypes, slight methyl methanesulfonate (MMS) sensitivity and reduction

128 ciency suppressed the camptothecin (CPT) and methyl methanesulfonate (MMS) sensitivity of nuclease-de

129 nt effect on a larval mitotic checkpoint and methyl methanesulfonate (MMS) sensitivity.

130 NA glycosylase (AAG), along with exposure to methyl methanesulfonate (MMS) to study mutagenesis as a

131 down S phase in response to hydroxy urea or methyl methanesulfonate (MMS) treatment.

132 ted BRCA2 were shown to be hypersensitive to methyl methanesulfonate (MMS) treatment.

133 ncreased sensitivity to the alkylating agent methyl methanesulfonate (MMS) was also observed for siRN

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

135 ction of the three major gadd transcripts by methyl methanesulfonate (MMS), and almost completely blo

136 usions, rad30 mutant cells were sensitive to methyl methanesulfonate (MMS), and rev1 rad30 or rev3 ra

137 e determined the mutation spectrum caused by methyl methanesulfonate (MMS), and showed that MMS also

138 unction, sensitivity to hydroxyurea (HU) and methyl methanesulfonate (MMS), and ubiquitination of pro

139 ferring resistance to the DNA-damaging agent methyl methanesulfonate (MMS), as determined by chemogen

140 after treatment with UV, mitomycin C (MC) or methyl methanesulfonate (MMS), as well as homologous rec

141 ts are hypersensitive to the genotoxic agent methyl methanesulfonate (MMS), but the molecular basis o

142 Alkylating agents, such as methyl methanesulfonate (MMS), damage DNA and activate t

143 amma-rays, ultraviolet (UV)-C radiation, and methyl methanesulfonate (MMS), indicating the broad rele

144 the mechanism by which a DNA damaging agent, methyl methanesulfonate (MMS), induces RTP801 transcript

145 A-damaging agents, including UV irradiation, methyl methanesulfonate (MMS), mitomycin C, phleomycin,

146 gadd7 RNA include alkylating agents, such as methyl methanesulfonate (MMS), N-methyl-N'-nitro-N-nitro

147 er exposure to hydrogen peroxide (H(2)O(2)), methyl methanesulfonate (MMS), or camptothecin by monito

148 X-rays, 4-nitroquinoline 1-oxide (4-NQO) and methyl methanesulfonate (MMS), or when an HO endonucleas

149 In the presence of the DNA-damaging agent methyl methanesulfonate (MMS), TOR-dependent cell surviv

150 In contrast, GADD45 induction by methyl methanesulfonate (MMS), UV radiation (UV), and me

151 ells are treated with the DNA-damaging agent methyl methanesulfonate (MMS), we carried out two-dimens

152 oli However, we found that in vivo repair of methyl methanesulfonate (MMS)-induced alkylation damage

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

154 at mutating H2B K111 impairs the response to methyl methanesulfonate (MMS)-induced DNA lesions and di

155 n-conjugating enzyme UBC13 (E2) and promotes methyl methanesulfonate (MMS)-induced PCNA polyubiquitin

156 rat gadd153 in all the c-myc transfectants, methyl methanesulfonate (MMS)-induced transcription of t

157 -/-) cells treated with the alkylating agent methyl methanesulfonate (MMS).

158 e of DNA-damaging alkylating agents, such as methyl methanesulfonate (MMS).

159 ced upon treatment with the alkylating agent methyl methanesulfonate (MMS).

160 cells after exposure to the alkylating agent methyl methanesulfonate (MMS).

161 4 degrees C but do not affect sensitivity to methyl methanesulfonate (MMS).

162 treatment of cells with the alkylating agent methyl methanesulfonate (MMS).

163 ically by SN2-type alkylating agents such as methyl methanesulfonate (MMS).

164 east cells treated with the alkylating agent methyl methanesulfonate (MMS).

165 enesis from DNA base damaging agents such as methyl methanesulfonate (MMS).

166 impaired when exposed to hydroxyurea (HU) or methyl methanesulfonate (MMS).

167 genome-wide screen for sensitivity to 0.001% methyl methanesulfonate (MMS).

168 n during recovery from DNA damage induced by methyl methanesulfonate (MMS).

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

170 nization on exposure to the alkylating agent methyl methanesulfonate (MMS).

171 odulate the toxicity of the alkylating agent methyl methanesulfonate (MMS).

172 matically after treatment with the genotoxin methyl methanesulfonate (MMS).

173 n in yeast treated with the alkylating agent methyl methanesulfonate (MMS).

174 e sensitive to ultraviolet (UV) light and to methyl methanesulfonate (MMS).

175 onofunctional DNA methylating agents such as methyl methanesulfonate (MMS).

176 genetic background results in sensitivity to methyl methanesulfonate (MMS).

177 ined the progression of replication forks in methyl-methanesulfonate (MMS)-damaged cells, under diffe

178 ion factors (TFs) after exposure of yeast to methyl-methanesulfonate (MMS).

179 d missense umuD' mutants deficient in UV and methyl methanesulfonate mutagenesis.

180 d a 5- to 10-fold increase in sensitivity to methyl methanesulfonate, N-methyl-N-nitrosourea, and the

181 lm cDNA partially rescued the sensitivity to methyl methanesulfonate of Saccharomyces cerevisiae sgs1

182 h other and promote resistance to killing by methyl methanesulfonate, one gene (EGL1) previously iden

183 M block in isc1Delta cells when treated with methyl methanesulfonate or HU.

184 deubiquitinated when cells are treated with methyl methanesulfonate or hydrogen peroxide.

185 y after treatment with the alkylating agents methyl methanesulfonate or methyl nitrosourea.

186 e identical in their sensitivities to either methyl methanesulfonate or UV radiation treatment and in

187 apoptosis by GADD34 following treatment with methyl-methanesulfonate or ionizing radiation in HEK293

188 ad no effect on sensitivity to UV radiation, methyl methanesulfonate, or quinolone antibiotics.

189 Furthermore, methyl methanesulfonate reduced NAD(P)H in PARP-1+/+ cel

190 R/DR5 occurs in p53 wild-type cells, whereas methyl methanesulfonate regulation of KILLER/DR5 occurs

191 Cells when treated with methyl methanesulfonate resulted in foci containing AAG

192 However, treatment with methyl methanesulfonate resulted in three- to fourfold m

193 is to isolate 10 cold-sensitive (Cs-) and 31 methyl methanesulfonate-sensitive (Mmss) mutations of th

194 Expression of the mouse cDNA rescued the methyl methanesulfonate-sensitive phenotype in rad50 mut

195 owever, the rdh54 null mutation enhances the methyl methanesulfonate sensitivity of a rad54 mutant an

196 nopus cDNAs complemented the temperature and methyl methanesulfonate sensitivity of a yeast rad27 del

197 he acetylatable lysines of H3 for heightened methyl methanesulfonate sensitivity to be observed.

198 these mutant alleles exhibited higher UV and methyl methanesulfonate sensitivity, increased rates of

199 n GCR mutator strains also slightly enhanced methyl methanesulfonate sensitivity.

200 tes and resistance to the DNA damaging agent methyl methanesulfonate, suggesting this pathway negativ

201 th lipopolysaccharide were more resistant to methyl methanesulfonate than untreated cells.

202 responses of cells to the DNA-damaging agent methyl methanesulfonate, the replication inhibitor hydro

203 erfering RNA renders HeLa cells sensitive to methyl methanesulfonate treatment by a mechanism of shor

204 in response to DNA damage induced by either methyl methanesulfonate treatment or ionizing radiation,

205 ith human mutant M(krk) survived poorly upon methyl methanesulfonate treatment or when they were incu

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

207 eous chromosomal breaks and are sensitive to methyl methanesulfonate treatment.

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

209 s are hypersensitive to the alkylating agent methyl methanesulfonate, which creates DNA damage that i

210 For methyl methanesulfonate, which does not sequence selecti

211 cisplatin, benzo[a]pyrene diol epoxide, and methyl methanesulfonate, without intrinsic cytotoxicity.