Human DNA Repair Genes
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TLDR
Modulation of DNA repair should lead to clinical applications including improvement of radiotherapy and treatment with anticancer drugs and an advanced understanding of the cellular aging process.Abstract:
Cellular DNA is subjected to continual attack, both by reactive species inside cells and by environmental agents. Toxic and mutagenic consequences are minimized by distinct pathways of repair, and 130 known human DNA repair genes are described here. Notable features presently include four enzymes that can remove uracil from DNA, seven recombination genes related to RAD51, and many recently discovered DNA polymerases that bypass damage, but only one system to remove the main DNA lesions induced by ultraviolet light. More human DNA repair genes will be found by comparison with model organisms and as common folds in three-dimensional protein structures are determined. Modulation of DNA repair should lead to clinical applications including improvement of radiotherapy and treatment with anticancer drugs and an advanced understanding of the cellular aging process.read more
Citations
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MicroRNAs down-regulate homologous recombination in the G1 phase of cycling cells to maintain genomic stability
Young Eun Choi,Yunfeng Pan,Eunmi Park,Panagiotis A. Konstantinopoulos,Subhajyoti De,Alan D. D'Andrea,Dipanjan Chowdhury +6 more
TL;DR: In this article, a gain-of-function screen was conducted to identify miRNAs that regulate homologous recombination-mediated repair of DNA double-strand break (DSB)s.
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Genetic polymorphisms in DNA base-excision repair genes ADPRT, XRCC1, and APE1 and the risk of squamous cell carcinoma of the head and neck.
Chunying Li,Zhibin Hu,Jiachun Lu,Zhensheng Liu,Li E. Wang,Adel K. El-Naggar,Erich M. Sturgis,Margaret R. Spitz,Qingyi Wei +8 more
TL;DR: No reported studies have investigated the association between ADPRT and APE1 variants and SCCHN risk, and genetic variations in the genes encoding for these DNA repair enzymes may alter their functions.
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Base excision repair fidelity in normal and cancer cells
TL;DR: Recent studies have indicated that expression of some Pol beta variants or changes in expression of wild-type Pol beta protein, frequently found in cancer cells, can lead to DNA repair synthesis errors and confers to cells a mutator phenotype.
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The modified human DNA repair enzyme O(6)-methylguanine-DNA methyltransferase is a negative regulator of estrogen receptor-mediated transcription upon alkylation DNA damage.
TL;DR: The modified human DNA repair enzyme R-MGMT, formed from the suicidal repair of the mutagenic O 6-alkylguanine (6RG) lesions by MGMT in the cells exposed to alkylating carcinogens, functions in such control by preventing the estrogen receptor (ER) from transcription activation that mediates cell proliferation.
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Deficient nucleotide excision repair capacity enhances human prostate cancer risk.
Jennifer J. Hu,M. Craig Hall,Lawrence Grossman,Mohammad Hedayati,David L. McCullough,Kurt Lohman,L. Douglas Case +6 more
TL;DR: This pilot study is the first direct evidence associating deficient NERC with human CaP risk, measured by a plasmid-based host reactivation assay using cryopreserved lymphocytes collected in an ongoing, clinic-based case-control study.
References
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Quality control by DNA repair.
Tomas Lindahl,Richard D. Wood +1 more
TL;DR: In some cases, DNA damage is not repaired but is instead bypassed by specialized DNA polymerases, and the integrity of the genetic information is compromised.