Molecular mechanism of DNA deadenylation by the neurological disease protein aprataxin
about
The mechanism of double-strand DNA break repair by the nonhomologous DNA end-joining pathwayKinetic mechanism of human DNA ligase I reveals magnesium-dependent changes in the rate-limiting step that compromise ligation efficiencyRepair of persistent strand breaks in the mitochondrial genomeCrystal structures of aprataxin ortholog Hnt3 reveal the mechanism for reversal of 5'-adenylated DNAStructure of an aprataxin–DNA complex with insights into AOA1 neurodegenerative diseaseAprataxin 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 repairResonance assignment for a particularly challenging protein based on systematic unlabeling of amino acids to complement incomplete NMR data sets.Nonhomologous end joining: a good solution for bad endsStructural insights into NHEJ: building up an integrated picture of the dynamic DSB repair super complex, one component and interaction at a timeDNA repair deficiency in neurodegeneration.XRCC4 and XLF form long helical protein filaments suitable for DNA end protection and alignment to facilitate DNA double strand break repair.Expression of a pathogenic mutation of SOD1 sensitizes aprataxin-deficient cells and mice to oxidative stress and triggers hallmarks of premature ageing.Neurological disorders associated with DNA strand-break processing enzymes.Aprataxin localizes to mitochondria and preserves mitochondrial functionRecognition and repair of chemically heterogeneous structures at DNA endsMolecular underpinnings of Aprataxin RNA/DNA deadenylase function and dysfunction in neurological disease.Detection and repair of ionizing radiation-induced DNA double strand breaks: new developments in nonhomologous end joining.DNA damage and its links to neurodegeneration.The impact of base excision DNA repair in age-related neurodegenerative diseasesSynergistic decrease of DNA single-strand break repair rates in mouse neural cells lacking both Tdp1 and aprataxin.
P2860
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P2860
Molecular mechanism of DNA deadenylation by the neurological disease protein aprataxin
description
2008 nî lūn-bûn
@nan
2008 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2008 թվականի դեկտեմբերին հրատարակված գիտական հոդված
@hy
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
name
Molecular mechanism of DNA deadenylation by the neurological disease protein aprataxin
@ast
Molecular mechanism of DNA deadenylation by the neurological disease protein aprataxin
@en
Molecular mechanism of DNA deadenylation by the neurological disease protein aprataxin
@nl
type
label
Molecular mechanism of DNA deadenylation by the neurological disease protein aprataxin
@ast
Molecular mechanism of DNA deadenylation by the neurological disease protein aprataxin
@en
Molecular mechanism of DNA deadenylation by the neurological disease protein aprataxin
@nl
prefLabel
Molecular mechanism of DNA deadenylation by the neurological disease protein aprataxin
@ast
Molecular mechanism of DNA deadenylation by the neurological disease protein aprataxin
@en
Molecular mechanism of DNA deadenylation by the neurological disease protein aprataxin
@nl
P2860
P356
P1476
Molecular mechanism of DNA deadenylation by the neurological disease protein aprataxin
@en
P2093
P2860
P304
33994-34001
P356
10.1074/JBC.M807124200
P407
P577
2008-10-03T00:00:00Z