Repair and mutagenic potency of 8-oxoG:A and 8-oxoG:C base pairs in mammalian cells.
about
Long-patch DNA repair synthesis during base excision repair in mammalian cellsMutations induced by 8-hydroxyguanine (8-oxo-7,8-dihydroguanine), a representative oxidized base, in mammalian cellsA switch between DNA polymerases δ and λ promotes error-free bypass of 8-oxo-G lesionshMYH cell cycle-dependent expression, subcellular localization and association with replication foci: evidence suggesting replication-coupled repair of adenine:8-oxoguanine mispairsParkinson's disease brain mitochondria have impaired respirasome assembly, age-related increases in distribution of oxidative damage to mtDNA and no differences in heteroplasmic mtDNA mutation abundanceThe role of mismatch repair in the prevention of base pair mutations in Saccharomyces cerevisiae.Base excision repair capacity in informing healthspan.Recent aspects of oxidative DNA damage: guanine lesions, measurement and substrate specificity of DNA repair glycosylases.New paradigms in the repair of oxidative damage in human genome: mechanisms ensuring repair of mutagenic base lesions during replication and involvement of accessory proteins.Cancer-associated variants and a common polymorphism of MUTYH exhibit reduced repair of oxidative DNA damage using a GFP-based assay in mammalian cells.Transcription coupled repair of 8-oxoguanine in murine cells: the ogg1 protein is required for repair in nontranscribed sequences but not in transcribed sequences.Differential subcellular localization of human MutY homolog (hMYH) and the functional activity of adenine:8-oxoguanine DNA glycosylase.Poly(ADP-ribose) polymerase-1 (PARP-1) is required in murine cell lines for base excision repair of oxidative DNA damage in the absence of DNA polymerase beta.The R- and S-diastereoisomeric effects on the guanidinohydantoin-induced mutations in DNA.Altered minor-groove hydrogen bonds in DNA block transcription elongation by T7 RNA polymerase.Unlike catalyzing error-free bypass of 8-oxodGuo, DNA polymerase λ is responsible for a significant part of Fapy·dG-induced G → T mutations in human cells.Evidence of reactive oxygen species-mediated damage to mitochondrial DNA in children with typical autism.
P2860
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P2860
Repair and mutagenic potency of 8-oxoG:A and 8-oxoG:C base pairs in mammalian cells.
description
1998 nî lūn-bûn
@nan
1998年の論文
@ja
1998年論文
@yue
1998年論文
@zh-hant
1998年論文
@zh-hk
1998年論文
@zh-mo
1998年論文
@zh-tw
1998年论文
@wuu
1998年论文
@zh
1998年论文
@zh-cn
name
Repair and mutagenic potency of 8-oxoG:A and 8-oxoG:C base pairs in mammalian cells.
@en
Repair and mutagenic potency of 8-oxoG:A and 8-oxoG:C base pairs in mammalian cells.
@nl
type
label
Repair and mutagenic potency of 8-oxoG:A and 8-oxoG:C base pairs in mammalian cells.
@en
Repair and mutagenic potency of 8-oxoG:A and 8-oxoG:C base pairs in mammalian cells.
@nl
prefLabel
Repair and mutagenic potency of 8-oxoG:A and 8-oxoG:C base pairs in mammalian cells.
@en
Repair and mutagenic potency of 8-oxoG:A and 8-oxoG:C base pairs in mammalian cells.
@nl
P2093
P2860
P356
P1476
Repair and mutagenic potency of 8-oxoG:A and 8-oxoG:C base pairs in mammalian cells.
@en
P2093
P2860
P304
P356
10.1093/NAR/26.5.1276
P407
P577
1998-03-01T00:00:00Z