Biology subjects

lu, x.

Publications and source records attributed to lu, x..

3 recordsLinked to original sources

bioRxiv2025

A Gm6AG-binding protein from Vibrio cholerae.

Most known modification-dependent restriction endonucleases target 5-methylcytosine, only a few N6-methyladenine (6mA)-dependent restriction endonucleases have been well-characterized, and the majority of them recognize the G6mATC motif (e.g., DpnI, HHPV4I). Here, we report the identification of a novel 6mA-dependent DNA-binding protein from Vibrio cholerae, VchI, which specifically recognizes the G6mAG motif. VchI contains a winged helix (wH) domain that is homologous to the wH domain in DpnI. However, several key residues involved in 6mA recognition differ between VchI and DpnI, which may contribute to the discrepancy in their recognition specificities. These findings advance our understanding of prokaryotic 6mA modification diversity and the 6mA recognition mechanism of the wH domain, while simultaneously providing an innovative tool for epigenetic research.

biochemistry↗

bioRxiv2021

Nrf2 mediated ER-phagy protects against oxidative damage in intervertebral disc degeneration

Intervertebral disc degeneration (IDD) increases the risk of low back pain (LBP). Oxidative stress may induce cellular damage and contribute to various diseases including IDD. Endoplasmic reticulum autophagy (ER-phagy) is a specific type of autophagy, its role in oxidative stress induced damage as well as in IDD is unknown. This study explores the role of ER-phagy in oxidative damage in intervertebral disc nucleus pulposus cells (NPCs), as well as the Nrf2/FAM134B axis in ER-phagy regulation and IDD therapy. We found ER-phagy was decreased in NPCs during oxidative stress; while FAM134B may promote ER-phagy and alleviate oxidative stress induced ER-stress and apoptosis. In addition, the nuclear transcription factor Nrf2 may promote the expression of FAM134B as well as ER-phagy, and suppress ER-stress and apoptosis in NPCs. Furthermore, overexpression of FAM134B and Nrf2 could effectively attenuate the progression of IDD in rats in vivo. These results suggest Nrf2/FAM134B mediated ER-phagy may combat oxidative damage in cells; meanwhile, ER-phagy as well as Nrf2 could be potential therapeutic targets for IDD. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=114 SRC="FIGDIR/small/469451v1_ufig1.gif" ALT="Figure 1"> View larger version (44K): org.highwire.dtl.DTLVardef@188b390org.highwire.dtl.DTLVardef@1c4e4f6org.highwire.dtl.DTLVardef@193fe77org.highwire.dtl.DTLVardef@12770e2_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗

bioRxiv2020

Identification and characterization of the hypoxia response regulatory elements in the accessible genome

Hypoxia is commonly observed in the solid tumor and contributes to the drug resistance in cancer therapy. Deciphering the epigenetic feature under the hypoxia condition in the solid tumor is critical for us to understand the tumorigenesis and design the precision therapy. Using the time series of ATAC-seq data under the hypoxia treatment from the epithelia cells, we identified the hypoxia response regulatory elements (HRREs) in the accessible genome. We found that these different HRREs have unique genomic features and are enriched with different transcriptional factors (TFs). Our study provides insights into the chromatin structure response to the hypoxia treatment and identifies useful genomic features for a better understanding of the hypoxia biology in the solid tumor.

cancer biology↗