ライフサイエンスコーパス: methyl methanesulfonate

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

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

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

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

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

6 tant cells treated with the alkylating agent methyl methanesulfonate.

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

8 serum deprivation and DNA damage elicited by methyl methanesulfonate.

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

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

11 e to the monofunctional DNA alkylating agent methyl methanesulfonate.

12 orodeoxyuridine, ethyl methanesulfonate, and methyl methanesulfonate.

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

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

15 prolonged exposure at high concentrations of methyl methanesulfonate.

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

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

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

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

20 eatment with rapamycin, hydrogen peroxide or methyl methanesulfonate.

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

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

23 cerevisiae treated with the alkylating agent methyl methanesulfonate.

24 sensitive to treatment with mitomycin C and methyl methanesulfonate.

25 ypersensitivity to the DNA-methylating agent methyl methanesulfonate.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

50 In both methyl methanesulfonate and UV survival experiments the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

149 4 degrees C but do not affect sensitivity to methyl methanesulfonate (MMS).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

191 For methyl methanesulfonate, which does not sequence selecti