Project description:Intense ultraviolet (UV) exposure can cause phototoxic reactions, such as skin inflammation, resulting in injury. UV is believed to be the direct cause of DNA damage, but the mechanisms of transcriptional regulation within cells after DNA damage are unclear. The bioinformatic analysis of transcriptome sequencing data from UV-irradiated and non-UV-irradiated skin showed that transcription-related proteins, such as HSF4 and COIL, mediate the cellular response to UV irradiation. HSF4 and COIL could form a complex under UV irradiation, and the preference for binding target genes changed. This is due to the presence of a large number of R-loops in the cells under UV irradiation and the ability of COIL to recognize the R-loops. The regulation of target genes was altered by the HSF4-COIL complex, and the expression of inflammation and aging-related genes, such as ATG7, TFPI, and LIMS1, were enhanced. A drug screen was performed for the recognition sites of COIL and R-loop. N6-(2-hydroxyethyl)-adenosine (HEA) could competitively bind COIL and inhibit the binding of COIL to R-loop. Thus, the activation of downstream inflammation-related genes and inflammatory skin injury were inhibited.
Project description:Analysis of Immediate Early Response 2 (Ier2)-inducible NIH 3T3 cells after Ier2 induction with RheoSwitch ligand RSL-1. Results provide insight into the function of Ier2 in NIH 3T3 mouse embryonal fibroblasts. Immediate early genes, including Ier2, are rapidly induced in quiescent cells by proliferation and migration-inducing stimuli. Microarray gene expression profiling was performed to identify differentially expressed genes following overexpression of Ier2 in NIH 3T3-Ier2 inducible cells after 24 hour induction of Ier2.
Project description:Expression profiling of HepG2 human liver carcinoma cells and NIH 3T3 mouse fibroblasts after arsite treatment for 24h. RNA-seq data comprise 4 groups: NIH 3T3 mouse fibroblasts control and arsite treatment, and HepG2 human liver carcinoma cells control and arsenite treatment. Jena Centre for Systems Biology of Ageing - JenAge (www.jenage.de)
Project description:DUBs exert their biological functions through specific substrates. Theoretically, as a substrate protein of JOSD2, its ubiquitination will be cut by JOSD2. In this regard, an analysis of ubiquitinome assay was performed to identify the potential substrates of JOSD2 in NIH/3T3 cells transfected with Flag-vector or Flag-JOSD2 plasmids.