Project description:Human myofibroblastic LX2 cells were transfected using a siRNA directed against BNC2 (siBNC2) or a control siRNA (siCTRL) and RNA were processed for microarray analyses.
Project description:The goal of this study was to use Rapid Immunoprecipitation Mass spectrometry of Endogenous protein (RIME) assays (Mohammed et al., 2016) to identify transcriptional regulatory partners of the transcription factor BNC2 in LX2 cells. Protein complexes were immune-precipitated with an anti-BNC2 antibody (55220-1-AP, Proteintech) or control non-immune IgG (normal rabbit IgG #2729, Cell Signaling) before being subjected to MS.
Project description:Mouse myofibroblastic EMS404 cells were transfected using a siRNA directed against BNC2 (siBNC2) or a control siRNA (siCTRL) and RNA were processed for microarray analyses.
Project description:Suberoylanilide hydroxamic acid (SAHA) and valproic acid (VPA) are both histone deacetylases inhibitor (HDACi), and are able to attenuate the activation of hepatic stelllate cells. To explore the underlying molecular mechanisms, we performed gene expression profile analyses of human hepatic stellate cell line LX2 treated with SAHA or VPA for 24 hours. Duplicate experiments were performed: Untreated LX2, SAHA treated LX2 and VPA treated LX2.
Project description:To investigate the mechanism of anti-fibrotic effect of ginkgetin, we performed gene expression profiling analysis using data obtain from RNA-seq of LX2 cells.
Project description:Suberoylanilide hydroxamic acid (SAHA) and valproic acid (VPA ) are both histone deacetylases inhibitor (HDACi), and are able to attenuate the activation of hepatic stelllate cells. To explore the underlying molecular mechanisms, we performed miRNA expression profile analyses of human hepatic stellate cell line LX2 treated with SAHA or VPA for 24 hours. Duplicate experiments were performed: Untreated LX2, SAHA treated LX2 and VPA treated LX2.
Project description:The communacation between the Hepatocellular carcinoma (HCC) and hepatic stellate cells(HSC) is not completely understood. Then a tumor-on-a-chip model was used to evaluate the crosstalk between the HCC cells (HCCLM3) and HSCs (LX2). After 5 days co-culture, we degraded the collagen hydrogel to isolate HCCLM3 cells and LX2 cells for RNA-seq.
