Journal ArticleDOI
Single-strand break repair and genetic disease
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TLDR
The molecular mechanisms and organization of the DNA-repair pathways that remove single-strand breaks are reviewed and the connection between defects in these pathways and hereditary neurodegenerative disease are discussed.Abstract:
Hereditary defects in the repair of DNA damage are implicated in a variety of diseases, many of which are typified by neurological dysfunction and/or increased genetic instability and cancer. Of the different types of DNA damage that arise in cells, single-strand breaks (SSBs) are the most common, arising at a frequency of tens of thousands per cell per day from direct attack by intracellular metabolites and from spontaneous DNA decay. Here, the molecular mechanisms and organization of the DNA-repair pathways that remove SSBs are reviewed and the connection between defects in these pathways and hereditary neurodegenerative disease are discussed.read more
Citations
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Journal ArticleDOI
XRCC1-mediated repair of strand breaks independent of PNKP binding.
Julie K. Horton,Donna F. Stefanick,Ming-Lang Zhao,Agnes K. Janoshazi,Natalie R. Gassman,Hannah J. Seddon,Samuel H. Wilson +6 more
TL;DR: Recruitment of additional fluorescently-tagged repair factors PARP-1-YFP, GFF-XRCC1, PNKP-GFP and Tdp1- GFP to micro-irradiation induced damage was assessed in wild-type XR CC1-expressing cells, and the similar half-times of recruitment suggest that XRCC 1 may be recruited with other proteins possibly as a pre-formed complex.
Journal ArticleDOI
Atm deficiency in the DNA polymerase β null cerebellum results in cerebellar ataxia and Itpr1 reduction associated with alteration of cytosine methylation.
TL;DR: A new murine model of cerebellar ataxia resulting from concomitant inactivation of POLB and ATM is reported, suggesting that dysregulation of ITPR1 in the cerebellum could be one of contributing factors to progressive ataxIA observed in human genomic instability syndromes.
Journal ArticleDOI
Down-regulation of ERK1/2 and AKT-mediated X-ray repair cross-complement group 1 protein (XRCC1) expression by Hsp90 inhibition enhances the gefitinib-induced cytotoxicity in human lung cancer cells.
Chun-Liang Tung,Yi-Jun Jian,Jhan-Jhang Syu,Tai-Jing Wang,Po-Yuan Chang,Chien-Yu Chen,Yun-Ting Jian,Yun-Wei Lin +7 more
TL;DR: It is suggested that down-regulation of XRCC1 can enhance the sensitivity of gefitinib for NSCLC cells.
Journal ArticleDOI
A universal sensing platform based on the repair ligation-mediated light-producing DNA machine
TL;DR: The repair ligation-mediated light-producing DNA machine can produce light through transforming the repetitive DNA cleavage/ligation motions into optical energy without the requirement of either external reporting reagents or excitation light.
Book ChapterDOI
Photoinduced damage resulting from fluorescence imaging of live cells.
TL;DR: In this paper, the authors examine potential live cell damage by first discussing common imaging considerations and modalities in fluorescence microscopy, and then consider several mechanisms by which various photochemical and photophysical phenomena cause cellular damage and introduce techniques that have leveraged these phenomena to intentionally create damage inside cells.
References
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Journal ArticleDOI
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Journal ArticleDOI
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Journal ArticleDOI
Oxidative Strand Scission of Nucleic Acids: Routes Initiated by Hydrogen Abstraction from the Sugar Moiety.
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