Project description:A CNC-family transcription factor, Nrf3, is highly expressed in the basal cell layer of the epidermis where melanocytes resident, although the melanogenic function of Nrf3 remains unclear. We used microarrays to identify NRF3-regulated gene expression network related to melanogenesis.
Project description:The genetic association of a transcription factor NRF3 with obesity has been reported, although the molecular mechanisms remain unknown We used microarrays to identify NRF3-regulated gene expression network related to lipid metabolism.
Project description:Accumulated evidences suggest physiological relevance between the transcription factor NRF3 (NFE2L3) and cancers. However NRF3 target genes in cancer cells remain poorly understood. We used microarrays to identify to identify NRF3 taget genes which regulate cell proliferation.
Project description:Neointimal hyperplasia (NIH), driven by vascular smooth muscle cell (VSMC) dysfunction, is a key factor in vascular diseases like atherosclerosis and restenosis. While Nrf3 is known to regulate VSMC differentiation, its role in NIH remains unclear. Using transcriptomic data, Nrf3 knockout mice (global), we assessed Nrf3’s impact on VSMC function and NIH. We identified Trim5, a gene linked to coronary artery disease, as a downstream target of Nrf3, which promotes autophagy in VSMCs and injured arteries, enhancing VSMC dysfunction and NIH. Nrf3 overexpression increased VSMC proliferation, migration, and inflammation, while deletion or knockdown had the opposite effects. Nrf3-/- and Nrf3ΔSMC mice showed reduced VSMC accumulation and attenuated NIH after vascular injury. These findings highlight Nrf3 as a novel modulator of VSMC dysfunction and injury-induced NIH, with potential for therapeutic targeting of the Nrf3-Trim5 axis to treat NIH-related vascular diseases.
Project description:We identified a tumor-suppressing function of NRF3 in skin cancer. To determine the underlying mechanism of action we wanted to compare the transcriptome of SCC13 NRF3-KO cells and SCC13 cells that re-express endogenous concentrations of recombinant NRF3.
Project description:HEK 293 cells with or without overexpression of ICER IIg were treated with forskolin for 0, 1 h, 2 h, 4 h or 8 h. The cell line used in the experiments is HEK 293 cells stable transfected with tetracycline-inducible ICER (Inducible cAMP early repressor) expression.
Project description:The aim of the study was to gain mechanistic insights of the protective effect of forskolin on thapsigargin-induced podocyte death by assessing, analyzing and comparing the respective gene expression profiles.
Project description:We identified the transcription factor NRF3 as an important tumor-suppressing protein in the skin. To gain insight into the mechanisms of action of NRF3 in keratinocytes, we searched for NRF3 interactors in the SCC13 skin cancer and the immortalized non-tumorigenic HaCaT cell line using BioID interaction screening.