DNA repair of clustered lesions in mammalian cells: involvement of non-homologous end-joining.
about
The functional landscape of Hsp27 reveals new cellular processes such as DNA repair and alternative splicing and proposes novel anticancer targetsDNA double-strand-break complexity levels and their possible contributions to the probability for error-prone processing and repair pathway choiceDNA Polymerases λ and β: The Double-Edged Swords of DNA RepairApex1 can cleave complex clustered DNA lesions in cells.Alkylation base damage is converted into repairable double-strand breaks and complex intermediates in G2 cells lacking AP endonuclease.DNA-PKcs deficiency leads to persistence of oxidatively induced clustered DNA lesions in human tumor cells.Saccharomyces cerevisiae-based system for studying clustered DNA damages.Requirements for 5'dRP/AP lyase activity in Ku.Clustered DNA lesion repair in eukaryotes: relevance to mutagenesis and cell survivalIrreparable complex DNA double-strand breaks induce chromosome breakage in organotypic three-dimensional human lung epithelial cell cultureFractionated Radiation Exposure of Rat Spinal Cords Leads to Latent Neuro-Inflammation in Brain, Cognitive Deficits, and Alterations in Apurinic Endonuclease 1.Mechanism of cluster DNA damage repair in response to high-atomic number and energy particles radiation.Specificity of the dRP/AP lyase of Ku promotes nonhomologous end joining (NHEJ) fidelity at damaged ends.Base damage immediately upstream from double-strand break ends is a more severe impediment to nonhomologous end joining than blocked 3'-terminiArtemis is required to improve the accuracy of repair of double-strand breaks with 5'-blocked termini generated from non-DSB-clustered lesions.Homologous recombination rescues ssDNA gaps generated by nucleotide excision repair and reduced translesion DNA synthesis in yeast G2 cells.The formation of double-strand breaks at multiply damaged sites is driven by the kinetics of excision/incision at base damage in eukaryotic cells.Replication fork collapse is a major cause of the high mutation frequency at three-base lesion clustersThe yield, processing, and biological consequences of clustered DNA damage induced by ionizing radiation.Reduced repair capacity of a DNA clustered damage site comprised of 8-oxo-7,8-dihydro-2'-deoxyguanosine and 2-deoxyribonolactone results in an increased mutagenic potential of these lesions.Resolution of complex ends by Nonhomologous end joining - better to be lucky than good?Evidence for double-strand break mediated mitochondrial DNA replication in Saccharomyces cerevisiae.Increased mutability and decreased repairability of a three-lesion clustered DNA-damaged site comprised of an AP site and bi-stranded 8-oxoG lesions.Hierarchy of lesion processing governs the repair, double-strand break formation and mutability of three-lesion clustered DNA damage.Ape1 guides DNA repair pathway choice that is associated with drug tolerance in glioblastomaProcessing of thymine glycol in a clustered DNA damage site: mutagenic or cytotoxic.Efficient processing of abasic sites by bacterial nonhomologous end-joining Ku proteins
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P2860
DNA repair of clustered lesions in mammalian cells: involvement of non-homologous end-joining.
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年論文
@yue
2008年論文
@zh-hant
2008年論文
@zh-hk
2008年論文
@zh-mo
2008年論文
@zh-tw
2008年论文
@wuu
2008年论文
@zh
2008年论文
@zh-cn
name
DNA repair of clustered lesion ...... of non-homologous end-joining.
@en
type
label
DNA repair of clustered lesion ...... of non-homologous end-joining.
@en
prefLabel
DNA repair of clustered lesion ...... of non-homologous end-joining.
@en
P2093
P2860
P356
P1476
DNA repair of clustered lesion ...... of non-homologous end-joining.
@en
P2093
Lynn Harrison
Reneau Castore
Svitlana Malyarchuk
P2860
P304
P356
10.1093/NAR/GKN450
P407
P577
2008-07-24T00:00:00Z