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1 ing genotoxins such as hydrogen peroxide and methylmethane sulfonate.
2  inhibitor hydroxyurea or DNA damaging agent methylmethane sulfonate.
3 DNA-damaging agents such as UV radiation and methylmethane sulfonate.
4 the zinc fingers themselves are sensitive to methylmethane sulfonate and have reduced ability to indu
5 reatment of cells with DNA alkylating agents methylmethane sulfonate and N-methyl-N'-nitro-N-nitrosog
6 tion in vitro, sensitize yeast to killing by methylmethane sulfonate and reduce spontaneous gene conv
7 te the cytotoxicity of the alkylating agents methylmethane sulfonate and temozolomide.
8 are sensitive both to the DNA damaging agent methylmethane sulfonate and to exposure to UV radiation.
9 eased sensitivity to the DNA-damaging agents methylmethane sulfonate and ultraviolet radiation.
10 DNA-damaging reagents including hydroxyurea, methylmethane sulfonate, and bleocin, demonstrating a ro
11 ons are hyperrecombinogenic and sensitive to methylmethane sulfonate, and they become inviable upon i
12 ain was sensitive to UV irradiation, X-rays, methylmethane sulfonate, and thiabendazole, and these se
13  models that predict cellular sensitivity to methylmethane sulfonate, H2O2, and 5-FU from DRC.
14 UV irradiation and to the DNA damaging agent methylmethane sulfonate, implying that DNA repair pathwa
15 l Fpg conferred Tpp1-dependent resistance to methylmethane sulfonate in yeast lacking the abasic endo
16 o fully rescue pol beta-deficient cells from methylmethane sulfonate-induced cytotoxicity.
17  therapeutic agents, including UV radiation, methylmethane sulfonate, ionizing radiation, etoposide,
18 53 during treatment with, and recovery from, methylmethane sulfonate-mediated DNA damage.
19 as PYK2, CADTK) is activated specifically by methylmethane sulfonate (MMS) and hyperosmolarity but no
20 ons and in response to the methylating-agent methylmethane sulfonate (MMS) and ionizing radiation.
21 ensitivity to the replication-blocking agent methylmethane sulfonate (MMS) in smc6 mutants, with doub
22 examined the effects of the alkylating agent methylmethane sulfonate (MMS) on gene expression in mous
23  induced in 32D cl3 myeloid cells exposed to methylmethane sulfonate (MMS), a DNA alkylating agent.
24 iminished G1 checkpoint after treatment with methylmethane sulfonate (MMS), a DNA base-damaging agent
25                           When etoposide and methylmethane sulfonate (MMS), both DNA damaging agents,
26 ferent mechanisms of action and DNA targets: methylmethane sulfonate (MMS), methylnitrosourea (MNU),
27                     Here we demonstrate that methylmethane sulfonate (MMS)-induced activation of JNK
28 ired in vivo for resistance to DNA damage by methylmethane sulfonate (MMS).
29 dc9 mutations, hydroxyurea, camptothecin, or methylmethane sulfonate (MMS).
30 d27 deletion mutants are highly sensitive to methylmethane sulfonate (MMS).
31 and hdf1delta strains were also sensitive to methylmethane sulfonate (MMS).
32  found that oxidation (H2O2) and alkylation (methylmethane sulfonate, MMS) stresses induced nearly id
33 oter reporter construct after treatment with methylmethane sulfonate or UV-radiation.
34 mage with H(2)O(2) or alkylation damage with methylmethane sulfonate, or rat lung fibroblasts after o
35       The pif1delta dna2delta strain remains methylmethane sulfonate sensitive and temperature sensit
36      In contrast, beta-only lyases increased methylmethane sulfonate sensitivity independently of Tpp
37 e-strand break and partially complements the methylmethane sulfonate sensitivity of the mutant cells.
38 xcision repair function, as evidenced by our methylmethane sulfonate sensitivity studies.
39 ellular resistance to the DNA damaging agent methylmethane sulfonate, suggesting that nucleotide bind
40 e found that Tpp1 could confer resistance to methylmethane sulfonate when expressed in bacteria that