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Cited by 178

The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.

hMutSα- and hMutLα-dependent phosphorylation of p53 in response to DNA methylator damage

Open access
Duckett, Derek R., Bronstein, S. Maynard, Taya, Yoichi, Modrich, Paul·1999·Proceedings of the National Academy of Sciences

Abstract

hMSH2⋅hMSH6 heterodimer (hMutSα) and hMLH1⋅hPMS2 complex (hMutLα) have been implicated in the cytotoxic response of mammalian cells to a number of DNA-damaging compounds, including methylating agents that produce O 6 -methylguanine (O 6 MeG) adducts. This study demonstrates that O 6 MeG lesions, in which the damaged base is paired with either T or C, are subject to excision repair in a reaction that depends on a functional mismatch repair system. Furthermore, treatment of human cells with the S N 1 DNA methylators N -methyl- N -nitrosourea or N -methyl- N′ -nitro- N -nitrosoguanidine results in p53 phosphorylation on serine residues 15 and 392, and these phosphorylation events depend on the presence of functional hMutSα and hMutLα. Coupled with the previous demonstration that O 6 MeG⋅T and O 6 MeG⋅C pairs are recognized by hMutSα, these results implicate action of the mismatch repair system in the initial step of a damage-signaling cascade that can lead to cell-cycle checkpoint activation or cell death in response to DNA methylator damage.

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Metadata

Authors
Duckett, D. R., Bronstein, S. M., Taya, Y., & Modrich, P.
Venue
Proceedings of the National Academy of Sciences
Published
1999-10-26
Volume
96
Issue
22
Pages
12384-12388
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W1692796156
Cited by
178
References
5
FWCI
6.09
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: hMutSα- and hMutLα-dependent phosphorylation of p53 in response to DNA methylator damage. https://app.cochat.ai/papers/10.1073/pnas.96.22.12384
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Duckett, D. R., Bronstein, S. M., Taya, Y., & Modrich, P. (1999). hMutSα- and hMutLα-dependent phosphorylation of p53 in response to DNA methylator damage. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.96.22.12384

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