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:Proteomics of HEPG2 cells following FTO overexpression and knockdown. Data accompany our paper entitled “Dynamic Regulation of N6,2′-O-dimethyladenosine (m6Am) in Obesity” scheduled for publication in Nature Communications, 2021
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.
Project description:Proteomes of Mycoplasma gallisepticum strains with overexpression and knockdown of WhiA transcription factor. The overexpression was introduced on a transposon vector carrying M. gallisepticum whiA gene with strong constitutive promoter and strong SD sequence. The knockdown was made by CRISPRi. dCas9 protein and sgRNA against whiA gene were introduced on a transposon vector.
Project description:The transcription factor HOXC6 is upregulated in human prostate cancer. SiRNA knockdown of HOXC6 induces apoptosis in LNCaP cells while upregulation rescued LNCaP cells from siRNA-induced apoptosis. We used microarrays to identify the genes whose expression underly the anti-apoptotic and proliferative effects of HOXC6 in LNCaP cells. Keywords: transient overexpression and knockdown
Project description:Acetylated proteome data of young human dermal fibroblasts (HDFs) [Young], old HDFs [Old], FTO-knockdown HDFs [shFTO], KAT8-overexpression HDFs [KAT8] and KAT8-overexpressed HDFs after FTO deprivation [shFTO_KAT8] were analysed by LC‒MS/MS.
Project description:NEDD9 is important for lung cancer metastasis. However, the detailed mechanism remains elusive. Using the microarray data generated with human lung cancer cell lines with either NEDD9 overexpression or NEDD9 knockdown, we plan to idnetify important signal pathways regulated by NEDD9. This may explain how NEDD9 excutes its function in lung cancer. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. Human lung cancer cell line A549, which has LKB1 loss-of-function mutation and increased expression of NEDD9, was used for two individual NEDD9 knockdown. Human lung cancer cell line CRL-5907, which has wild-type LKB1 and low NEDD9 expression level, was used for NEDD9 overexpression. The microarray was done in A549 cells, A549 cells with two different NEDD9 knockdown; CRL-5907 cells and CRL-5907 cells with NEDD9 overexpression.