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Newborn (Clarksville)
March 2024
Global Newborn Society, Clarksville Maryland, United States of America.
DNA Repair (Amst)
January 2024
Department of Urology, the First Affiliated Hospital of Xi'an Jiaotong University, China; Oncology Research Lab, Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education, #277 Yanta West Road, Xi'an 710061, China. Electronic address:
Zhonghua Gan Zang Bing Za Zhi
September 2023
Department of General Surgery, Lanzhou University Second Hospital, Lanzhou 730030, China.
To evaluate the role and molecular mechanism of Nei endonuclease VIII-like protein 3 (NEIL3) in hepatocellular carcinoma (HCC) through The Cancer Genome Atlas database. RNA sequencing of HCC samples was the first step in determining the level of gene NEIL3 expression in normal tissues and tumors. Then, NEIL3 was used for the Gene Ontology, the Kyoto Encyclopedia of Genes and Genomes, gene enrichment analysis, immune cell infiltration analysis.
View Article and Find Full Text PDFJ Neurochem
June 2023
Department of Physiology, National Cheng Kung University, Tainan, Taiwan.
Parkinson's disease (PD) is a common movement disorder caused by a characteristic loss of dopaminergic neurons in the substantia nigra and degeneration of dopamine terminals in the dorsal striatum. Previous studies have suggested that oxidative stress-induced DNA damage may be involved in PD pathogenesis, as steady-state levels of several types of oxidized nucleobases were shown to be elevated in PD brain tissues. These DNA lesions are normally removed from the genome by base excision repair, which is initiated by DNA glycosylase enzymes such as endonuclease VIII-like 1 (Neil1).
View Article and Find Full Text PDFPLoS One
March 2020
Department of Molecular Biology and Genetics.
Base excision repair (BER) defects and concomitant oxidative DNA damage accumulation play a role in the etiology and progression of late-onset Alzheimer's disease (LOAD). However, it is not known whether genetic variant(s) of specific BER genes contribute to reduced BER activity in LOAD patients and whether they are associated with risk, development and/or progression of LOAD. Therefore, we performed targeted next generation sequencing for three BER genes, uracil glycosylase (UNG), endonuclease VIII-like DNA glycosylase 1 (NEIL1) and polymerase β (POLβ) including promoter, exonic and intronic regions in peripheral blood samples and postmortem brain tissues (temporal cortex, TC and cerebellum, CE) from LOAD patients, high-pathology control and cognitively normal age-matched controls.
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