Synergistic decrease of DNA single-strand break repair rates in mouse neural cells lacking both Tdp1 and aprataxin.
about
CK2 phosphorylation-dependent interaction between aprataxin and MDC1 in the DNA damage responseRepair of persistent strand breaks in the mitochondrial genomeR-loops in proliferating cells but not in the brain: implications for AOA2 and other autosomal recessive ataxiasAprataxin resolves adenylated RNA–DNA junctions to maintain genome integrityGenetic interactions between HNT3/Aprataxin and RAD27/FEN1 suggest parallel pathways for 5' end processing during base excision repairATM deficiency results in accumulation of DNA-topoisomerase I covalent intermediates in neural cellsTyrosyl-DNA-phosphodiesterases (TDP1 and TDP2).Identification of novel PARP inhibitors using a cell-based TDP1 inhibitory assay in a quantitative high-throughput screening platform.DNA repair deficiency in neurodegeneration.Expression of a pathogenic mutation of SOD1 sensitizes aprataxin-deficient cells and mice to oxidative stress and triggers hallmarks of premature ageing.Non-homologous end joining: Common interaction sites and exchange of multiple factors in the DNA repair process.DNA repair mechanisms in dividing and non-dividing cells.Aprataxin localizes to mitochondria and preserves mitochondrial functionTyrosyl-DNA Phosphodiesterase 1 (Tdp1) inhibitorsDisconnecting XRCC1 and DNA ligase IIILack of aprataxin impairs mitochondrial functions via downregulation of the APE1/NRF1/NRF2 pathway.Tyrosyl-DNA phosphodiesterase 1 (TDP1) repairs DNA damage induced by topoisomerases I and II and base alkylation in vertebrate cells.Slow mitochondrial repair of 5'-AMP renders mtDNA susceptible to damage in APTX deficient cells.TDP2 promotes repair of topoisomerase I-mediated DNA damage in the absence of TDP1.DNA damage response.To live or to die: a matter of processing damaged DNA termini in neurons.Topoisomerase I inhibition in colorectal cancer: biomarkers and therapeutic targets.Resolution of complex ends by Nonhomologous end joining - better to be lucky than good?Tyrosyl-DNA phosphodiesterase I resolves both naturally and chemically induced DNA adducts and its potential as a therapeutic target.The role of DNA base excision repair in brain homeostasis and disease.Clinical and cellular roles for TDP1 and TOP1 in modulating colorectal cancer response to irinotecanChronic oxidative damage together with genome repair deficiency in the neurons is a double whammy for neurodegeneration: Is damage response signaling a potential therapeutic target?SUMO modification of the neuroprotective protein TDP1 facilitates chromosomal single-strand break repair.DNA end-processing enzyme polynucleotide kinase as a potential target in the treatment of cancer.TDP1/TOP1 Ratio as a Promising Indicator for the Response of Small Cell Lung Cancer to Topotecan.Complementation of aprataxin deficiency by base excision repair enzymes in mitochondrial extracts.DNA 3'-phosphatase activity is critical for rapid global rates of single-strand break repair following oxidative stress.Novel group of tyrosyl-DNA-phosphodiesterase 1 inhibitors based on disaccharide nucleosides as drug prototypes for anti-cancer therapy
P2860
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P2860
Synergistic decrease of DNA single-strand break repair rates in mouse neural cells lacking both Tdp1 and aprataxin.
description
2009 nî lūn-bûn
@nan
2009年の論文
@ja
2009年論文
@yue
2009年論文
@zh-hant
2009年論文
@zh-hk
2009年論文
@zh-mo
2009年論文
@zh-tw
2009年论文
@wuu
2009年论文
@zh
2009年论文
@zh-cn
name
Synergistic decrease of DNA si ...... cking both Tdp1 and aprataxin.
@en
type
label
Synergistic decrease of DNA si ...... cking both Tdp1 and aprataxin.
@en
prefLabel
Synergistic decrease of DNA si ...... cking both Tdp1 and aprataxin.
@en
P2093
P2860
P1433
P1476
Synergistic decrease of DNA si ...... cking both Tdp1 and aprataxin.
@en
P2093
Keith W Caldecott
Peter J McKinnon
Poorvi Patel
Sachin Katyal
Sherif F El-Khamisy
P2860
P304
P356
10.1016/J.DNAREP.2009.02.002
P577
2009-03-19T00:00:00Z