Project description:To interrogate occupany sites of Foxc1 transcription factor whole genome ChIP-sequencing was performed on Gli2-mGFP NIH3T3 reporter cells stably expressing Foxc1, using different anti-Foxc1 antibodies.
Project description:To identify pathways transcriptionally controlled by Foxc1, NIH3T3 fibroblasts stably overexpressing Foxc1 ORF, or an empty retroviral vector control, were subjected to RNA-sequencing.
Project description:To investigate biological function of MARVELD1, we have employed whole genome microarray expression profiling as a platform to analyze gene expression alternation influenced by MARVELD1. MARVELD1 stably transfected NIH3T3 and control vector cells were used to compare their gene expression profiling.
Project description:Chromatin immunoprecipitation using Foxc1 antibodies in second branchial arch (IIBA) cells from E11.5 mouse embryos detected by SOLiD sequencing
Project description:To investigate biological function of MARVELD1, we have employed whole genome microarray expression profiling as a platform to analyze gene expression alternation influenced by MARVELD1. MARVELD1 stably transfected NIH3T3 and control vector cells were used to compare their gene expression profiling. Total RNA from MARVELD1 overexpressing NIH3T3 cells and control cells were extracted to analyze their gene expression profiles by using mouse whole genome expression microarray.
Project description:Foxc1 has been identified to participate in regulating genes expression directly by binding their promoters as well as playing various roles in signal transduction within the cells. In this study, we found that, in F9 Embryonal Carcinoma cells, Foxc1 repressed the promoter’s transcription activity by binding the region of 1Kb upstream of Transcription Start Site within Nanog promoter.To understand more functions of Foxc1, streptavidin-biotin affinity purification combined with Liquid chromatography electrospray ionization tandem mass spectrometry (LC-ESI-MS/MS) analysis was carried out.Bioinformatic analysis identified 360 proteins which may act as Foxc1 interactors.
Project description:Aurintricarboxylic acid (ATA) was identified as a potent inhibitor of the TAZ/TEAD transcriptional complex via a Alpha-LISA screen. We have previously demonstrated that a hyperfunctional form of TAZ, TAZ-CAMTA1, is sufficient to induce the development of a rare vascular sarcoma, Epithelioid Hemangioendothelioma. We have demonstrated that TAZ-CAMTA1 can similarly transform NIH3T3 cells to yield anchorage independent growth in vitro and this action requires the formation of a TAZ-CAMTA1/TEAD complex. To identify if ATA is able to inhibit the transcriptional action TAZ-CAMTA1/TEAD complex, whole transcriptomic analysis was performed on TAZ-CAMTA1 stably transfected NIH3T3 cells with or without ATA.