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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Polymorphisms of the DNA repair genes XPD and XRCC1 and the risk of age-related cataract development in Han Chinese.
TL;DR: The results suggest that polymorphisms in XRCC1 codon 399 may be associated with the development of age-related cataract in Han Chinese.
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Cockayne Syndrome exhibits dysregulation of p21 and other gene products that may be independent of transcription coupled repair
TL;DR: It is found that the CSB defect results in altered expression of anti-angiogenic and cell cycle genes and proteins at the level of both gene expression and protein lifetime, and the complex symptoms of CS may be due to multiple, independent downstream targets of the E3 ubiquitylation system.
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Exonuclease 1 is a critical mediator of survival during DNA double strand break repair in nonquiescent hematopoietic stem and progenitor cells.
TL;DR: It is proposed Exo1‐mediated HR is dispensable for stem cell function in quiescent HSC, whereas it is essential to HSC response to DNA damage processing after cell cycle entry, and its loss is not compensated by intact NHEJ.
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Etiology of Acute Myeloid Leukemia in the Elderly
TL;DR: The increasing prevalence of deletional and complex karyotypes in elderly AML patients implies a cumulative genotoxicity over time for this subgroup, given the similar spectrum of abnormalities following exposure to known genotoxic agents such as alkylating chemotherapeutic drugs.
References
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Manel Esteller,Jesús García-Foncillas,Esther Andion,Steven N. Goodman,Oscar Fernandez Hidalgo,Vicente Vanaclocha,Stephen B. Baylin,James G. Herman +7 more
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TL;DR: A reusable library of bacterial clones is constructed that will permit unlimited RNAi screens in the future and should help develop a more complete view of the relationships between the genome, gene function and the environment.
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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.