Samuel H. Wilson

Publications462
h-index72
Citations16,660
Highly Influential Citations632
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OGG1 initiates age-dependent CAG trinucleotide expansion in somatic cells
TLDR
It is shown that the age-dependent somatic mutation associated with Huntington’s disease occurs in the process of removing oxidized base lesions, and is remarkably dependent on a single base excision repair enzyme, 7,8-dihydro-8-oxoguanine-DNA glycosylase (OGG1).
AP endonuclease-independent DNA base excision repair in human cells.
A role for p53 in base excision repair
TLDR
A novel role for p53 in DNA repair, which could contribute to its function as a key tumor suppressor and is supported by the facts that BER activity in human and murine cell extracts closely parallels their levels of endogenous p53, and that P53 activity is much reduced in cell extracts immunodepleted of p53.
Mammalian Abasic Site Base Excision Repair
TLDR
It is found that AP site BER can be reconstituted in vitro using the following purified human proteins: AP endonuclease, β-pol, and DNA ligase I and the potential significance of the dRP-containing intermediate in the regulation of BER is discussed.
In situ analysis of repair processes for oxidative DNA damage in mammalian cells.
TLDR
It is shown, in real time after irradiation by using antibodies and GFP-tagged proteins, rapid and ordered DNA repair processes of oxidative DNA damage in human cells, and that XRCC1 is essential for both polymerase beta-dependent and proliferating cell nuclear antigen-dependent repair pathways of single-strand breaks.
The lyase activity of the DNA repair protein β-polymerase protects from DNA-damage-induced cytotoxicity
TLDR
Results indicate that removal of the dRP group is a pivotal step in BER in vivo, which results in the hypersensitivity phenotype of β-pol null cells and may signal downstream events such as apoptosis and necrotic cell death.
FEN1 Stimulation of DNA Polymerase β Mediates an Excision Step in Mammalian Long Patch Base Excision Repair*
TLDR
It is demonstrated by immunodepletion experiments that 5′-dRP-N3excision in long patch BER of uracil-DNA in a human lymphoid cell extract is, indeed, dependent upon FEN1 and that human F EN1 and β-pol can cooperate in longPatch BER excision and specify the predominant excision product seen with a cell extract.
XRCC1 and DNA polymerase β in cellular protection against cytotoxic DNA single-strand breaks
TLDR
A strong correlation is observed between cellular sensitivity to MMS and the ability of cells to repair MMS-induced damage and PARP inhibition demonstrating that PARP-mediated poly(ADP-ribosyl)ation plays a role in modulation of cytotoxicity beyond recruitment of XRCC1 to sites of DNA damage.
Requirement of mammalian DNA polymerase-β in base-excision repair
TLDR
These studies demonstrate that β-polymerase functions specifically in base-excision repair in vivo, and establishes embryonic fibroblast cell lines homozygous for a deletion mutation in the gene encoding DNA polymerase-β.
NEIL2-initiated, APE-independent repair of oxidized bases in DNA: Evidence for a repair complex in human cells.
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