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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.
31 DNA-damaging agents (ultraviolet radiation, methyl methanesulfonate, adriamycin, camptothecin, and c
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
40 ase-deficient Escherichia coli cells against methyl methanesulfonate and hydrogen peroxide (H2O2) dam
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
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
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
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
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.
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
90 ts with the efficient repair of nonclustered methyl methanesulfonate-induced lesions, as measured by
92 exposing the cells to either hydroxyurea or methyl methanesulfonate, lending support for a DDK role
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
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
115 ciency suppressed the camptothecin (CPT) and methyl methanesulfonate (MMS) sensitivity of nuclease-de
117 NA glycosylase (AAG), along with exposure to methyl methanesulfonate (MMS) to study mutagenesis as a
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
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
138 ells are treated with the DNA-damaging agent methyl methanesulfonate (MMS), we carried out two-dimens
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
159 ined the progression of replication forks in methyl-methanesulfonate (MMS)-damaged cells, under diffe
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
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
172 R/DR5 occurs in p53 wild-type cells, whereas methyl methanesulfonate regulation of KILLER/DR5 occurs
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
181 tes and resistance to the DNA damaging agent methyl methanesulfonate, suggesting this pathway negativ
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
190 s are hypersensitive to the alkylating agent methyl methanesulfonate, which creates DNA damage that i
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