Project description:adenovirus mediated overexpression of wild-type CtBP2 and Rossmann fold mutant CtBP2 along with control GUS in dietary induced obese mice
Project description:Using an RNA interference-based genetic screen in mouse F9 cells we identify the transcriptional corepressor CTBP2 as a coactivator critically required for retinoic acid (RA)-induced transcription. Here we perfom a whole genome transcriptome analysis in F9 cells expressing shRNA for Ctbp2 and Rxr in the absence or presence of retinoic acid (RA). A total of 2,754 genes were found to be upregulated (>2 fold) and 1518 genes were downregulated (>2 fold) in response to RA treatment in the control cells. We find that around 52% and 55% of upregulated genes are dependent on Ctbp2 and Rxr for activation respectively suggesting that Ctbp2 is a coactivator of RA signaling. Whole genome RNA-sequencing in F9 cells expressing shGFP or shCtbp2 or shRxr
Project description:To discover the core gene expression features of CtBP1, CtBP2 differently regulated in ovarian cancer SKOV3 cells. The compared the whole transcript expression profiling between CtBP1 knockdown, CtBP2 knockdown and scramble control in ovarian cancer skov3 cells.
Project description:Using an RNA interference-based genetic screen in mouse F9 cells we identify the transcriptional corepressor CTBP2 as a coactivator critically required for retinoic acid (RA)-induced transcription. Here we perfom a whole genome transcriptome analysis in F9 cells expressing shRNA for Ctbp2 and Rxr in the absence or presence of retinoic acid (RA). A total of 2,754 genes were found to be upregulated (>2 fold) and 1518 genes were downregulated (>2 fold) in response to RA treatment in the control cells. We find that around 52% and 55% of upregulated genes are dependent on Ctbp2 and Rxr for activation respectively suggesting that Ctbp2 is a coactivator of RA signaling.
Project description:CTBP2 is a transcriptional co-repressor/co-activator palying a role in EMT. We have identified CTBP2 as a protein interacting with ZBTB18, a transcriptional repressor and tumor suppressor in GBM. Here, we have performed genome wide mapping of CTBP2 and ZBTB18 binding sites in GBM to characterized their gene regulation mechanism.
Project description:We have identified the CTBP2 protein as a new ZBTB18 interactor. Here we have evaluated transcriptomic changes upon CTBP2 knockdown in the GBM cell line SNB19. Moreover, we have analyzed whether CTBP2 is required for ZBTB18-mediated gene repression.