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Mechanisms involved in Helicobacter pylori-induced interleukin-8 production by a gastric cancer cell line, MKN45
TLDR
Results suggest that H. pylori induced the activation of NF-kappaB as well as AP-1, leading to IL-8 gene transcription, and mutation of the NF-IL6 binding site resulted in no decrease in the induction of luciferase activity.
Oxidative damage in nucleic acids and Parkinson's disease
TLDR
Significant increase in 8‐oxoG in mitochondrial DNA as well as an elevated expression of MTH1, OGG1, and MUTYH in nigrostriatal dopaminergic neurons of PD patients are shown, suggesting that the buildup of these lesions may cause dopamine neuron loss.
Two distinct pathways of cell death triggered by oxidative damage to nuclear and mitochondrial DNAs
TLDR
Both cell deaths were triggered by single‐strand breaks (SSBs) that had accumulated in the respective DNAs, and were suppressed by knockdown of adenine DNA glycosylase encoded by MutY homolog, thus indicating that excision ofAdenine opposite 8‐oxoG lead to the accumulation of SSBs in each type of DNA.
Hematopoietic tissue-specific expression of mouse Neil3 for endonuclease VIII-like protein.
TLDR
Cloned cDNA and genomic DNA containing exon 1 of mouse Neil3 and found candidate sequences for NEIL3 orthologues in a DNA database from dog and zebrafish in addition to human and mouse, but not invertebrates, may function exclusively in vertebrates, such as mammals.
APE1- and APE2-dependent DNA breaks in immunoglobulin class switch recombination
TLDR
It is shown that both APE1 and APE2 function in CSR, resulting in the DSBs necessary for CSR and thereby describing a novel in vivo function for APe2.
ITPase-deficient mice show growth retardation and die before weaning
TLDR
The role of ITPase in mice is to exclude ITP from the ATP pool, and the main target substrate of this enzyme is rITP, which suggests that cardiomyopathy is also caused by a defect in maintaining the quality of the ATP Pool, which is an essential requirement for sarcomere function.
8-Oxoguanine causes neurodegeneration during MUTYH-mediated DNA base excision repair.
TLDR
It is reported that neurodegeneration is triggered by MUTYH-mediated excision repair of 8-oxoG-paired adenine, and different signaling pathways were triggered by the accumulation of single-strand breaks in each type of DNA generated during base excison repair initiated by M UTYH, suggesting that suppression of MUTyH may protect the brain under conditions of oxidative stress.
Mutagenesis and carcinogenesis caused by the oxidation of nucleic acids
TLDR
Increased susceptibility to spontaneous carcinogenesis in MTH1-null mice is observed and MUTYH deficiency may increase G:C to T:A transversions through the misincorporation of 2-OH-dATP, especially in the intestinal tract.
Human APE2 protein is mostly localized in the nuclei and to some extent in the mitochondria, while nuclear APE2 is partly associated with proliferating cell nuclear antigen.
TLDR
The results suggest thatAPE2 participates in both nuclear and mitochondrial BER and also that nuclear APE2 functions in the PCNA-dependent BER pathway.
A genome-wide distribution of 8-oxoguanine correlates with the preferred regions for recombination and single nucleotide polymorphism in the human genome.
TLDR
It is demonstrated that 8-oxoG is unevenly distributed in the normal human genome and that the distribution pattern is conserved among different individuals, and regions with a high frequency of recombination and single nucleotide polymorphisms (SNPs) are preferentially located within chromosomal regions withA high density of 8-OxoG.
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