26 Papers
76 Citations
Zhen Yan is an academic researcher from Fourth Military Medical University. The author has contributed to research in topics: Hepatitis B virus & Cancer. The author has an hindex of 9, co-authored 26 publications.
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Papers
HBc binds to the CpG islands of HBV cccDNA and promotes an epigenetic permissive state.
TL;DR: Apparently, HBc is a positive regulator of HBV transcription and replication, maintaining the permissive epigenetic state in the critical region of the HBV cccDNA minichromosomes.
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Evidence that methylation of hepatitis B virus covalently closed circular DNA in liver tissues of patients with chronic hepatitis B modulates HBV replication.
TL;DR: The methylation level of the CpG island 2 of the ccc DNA in HBeAg‐negative patients was higher than that in H beAg‐positive patients, suggesting that HBV cccDNA methylation may be relevant to replication capability of HBV.
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A Novel Electrochemical Microfluidic Chip Combined with Multiple Biomarkers for Early Diagnosis of Gastric Cancer
TL;DR: The electrochemical microfluidic chip for detecting multiple biomarkers has great potential in applications such as early screening of Gastric cancer patients, and therapeutic evaluation, and real-time dynamic monitoring the progress of gastric cancer in near future.
Hepatitis B viral core protein disrupts human host gene expression by binding to promoter regions
Yanhai Guo,Wei Kang,Xiaoying Lei,Yongnian Li,An Xiang,Yonglan Liu,Jinrong Zhao,Ju Zhang,Zhen Yan +8 more
TL;DR: HBc has the ability to bind a large number of human gene promoters, and can disrupt normal host gene expression, and may represent a key pathogenic mechanism of HBV infection.
Alu RNA accumulation in hyperglycemia augments oxidative stress and impairs eNOS and SOD2 expression in endothelial cells
Wei Wang,Weihua Wang,Kazem M. Azadzoi,Peng Dai,Qin Wang,Jianbin Sun,Wentao Zhang,Yi Shu,Jing-Hua Yang,Jing-Hua Yang,Zhen Yan +10 more
TL;DR: This study uncovered endogenous Alu RNA accumulation in hyperglycemic endothelial cells that provoked endothelial oxidative stress and dysfunction by suppressing SOD2 and eNOS expression at both transcription and translation levels via NFκB signaling pathway.
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