Project description:expression profile of conditional knock out of beta-catenin by K19-CRE at E7.5. Tested a wild type with two alleles of beta-catenin, a heterzyote with one deleted allele and the conditional null in the domain on cytokeratin 19 driven CRE expression
Project description:expression profile of conditional knock out of beta-catenin by K19-CRE at E7.5. Tested a wild type with two alleles of beta-catenin, a heterzyote with one deleted allele and the conditional null in the domain on cytokeratin 19 driven CRE expression Keywords: other
2005-04-13 | GSE2519 | GEO
Project description:Beta catenin knock out in hESC
Project description:It has been shown that hypertrophic chondrocyte (HC) can become osteoblast, contributing to the formation of trabecular bone and endosteum. However, it is unclear what genes regulate the process of differentiation from chondrocyte to osteoblast. Conditional knock-out of β‑catenin in HCs can reduce the trabecular bone amount and there is also some evidence that ablation of β‑catenin in HCs can promote bone marrow adipogenesis. Conditional stabilization of β‑catenin in HCs results in osteopetrosis. In order to investigate the gene regulatory network with different dosage of β‑catenin in HC descendants (i.e. in Loss-of-Function mutant, Gain-of-Function mutant and Wildtype control), we collected HC descendant cells from proximal tibia of mice at postnatal day 5 and performed bulk RNA seq to profile the gene expression pattern in HC descendants.
Project description:The Wnt/β-catenin signalling pathway is a key regulator of embryonic stem cell self-renewal and differentiation. Constitutive activation of this pathway has been shown to significantly increase mouse embryonic stem cell (mESC) self-renewal and pluripotency marker expression. In this study, we generated a novel β-catenin knock-out model in mESCs by using CRISPR/Cas9 technology to delete putatively functional N-terminally truncated isoforms observed in previous knock-out models. While we showed that aberrant N-terminally truncated isoforms are not functional in mESCS, we observed that canonical Wnt signalling is not active in mESCs, as β-catenin ablation does not alter mESC transcriptional profile in LIF-enriched culture conditions; on the other hand, Wnt signalling activation represses mESC spontaneous differentiation. We also showed that transcriptionally silent β-catenin (ΔC) isoforms can rescue β-catenin knock-out self-renewal defects in mESCs, cooperating with TCF1 and LEF1 in the inhibition of mESC spontaneous differentiation in a Gsk3 dependent manner.
Project description:Conditional knock out of Brd1(bromodomain containing 1) in muse developmental T cells (CD4CD8DP, CD4SP and CD8SP) by intercrossing with Tie2-Cre Conditional knock out of Brd1(bromodomain containing 1) in muse MHC class l restricted T cells (CD8SP) by intercrossing with Tie2-Cre and OT-l Developmental T cells (defined by surface markers: CD4, CD8 and TCR?) derived from control (Tie2-Cre) or Brd1 conditional knock out (Brd1flox/flox, Tie2-Cre) thymocytes were isolated by fluorescence activated cell sorting (FACS) and subjected to a microarray analysis. CD8SP T cells were also isolated from control (Tie2-Cre, OT-l) or Brd1 conditional knock out (Brd1flox/flox, Tie2-Cre, OT-l) thymocytes intercrossed with OT-l.
Project description:Conditional knock out of Brd1(bromodomain containing 1) in muse developmental T cells (CD4CD8DP, CD4SP and CD8SP) by intercrossing with Tie2-Cre Conditional knock out of Brd1(bromodomain containing 1) in muse MHC class l restricted T cells (CD8SP) by intercrossing with Tie2-Cre and OT-l
Project description:To evaluate geneexpression profile in developing joints vs adjacent growth plate in control and TGF-beta type II receptor conditional knock-out in limb mesenchyjme
Project description:Brg1 has been reported to act as a trans-activator for the Wnt pathway by interacting with beta-catenin. Given this interaction and the crucial role Wnt signalling plays in the intestinal homeostasis, we aimed to investigate the effect of Brg1 loss on gene expression in normal and Wnt activated small intestinal epithelium. We used VillinCreERT2 Cre recombinase and loxP targeted allels of Brg1 and Apc to generate 4 cohorts of conditional knock-out mice: Cre-negative controls (n=4), Brg1 deficient (n=4), Apc deficient (n=3) and double Brg1-Apc deficient (n=4). All mice were induced by 4x80mg/kg daily injections of Tamoxifen. Epithelium enriched (gut scrapes) samples of small intestine (jejunum) were collected at day 4 post induction. Loss of Brg1 expression in the small intestinal epithelium at this time point was confirmed by immunohistochemistry.
Project description:β-Catenin is a regulator of cutaneous wound repair. The expression of genes that are modulated in response to changes in β-Catenin levels initiated prior to injury was investigated during the proliferative phase of repair. We are particularly interested in genes that are modulated (in opposite directions) in response to both the induction ('stabilization') versus downregulation of β-Catenin. To investigate this, conditional β-Catenin stabilized mice (Harada, N., et al. EMBO J. 1999 Nov 1;18(21):5931-42) were injected with either a Cre-expressing adenovirus, or a GFP-expressing control virus, four days prior to injury, and wounds were harvested eight days following injury. For conditional knockdown of β-Catenin, mice generated from a cross between conditional β-Catenin knockdown mice (Brault, V. et al., Development. 2001 Apr;128(8):1253-64), and mice that express a tamoxifen-inducible form of Cre (Hayashi, S., and McMahon, A.P., Dev Biol. 2002 Apr 15;244(2):305-18), were treated with Tamoxifen for five days prior to injury. Wounds were harvested eight days after wounding. This provides insight into gene expression changes that occur during the proliferative stage of cutaneous wound repair in response to changes in β-Catenin levels initiated before/at the time of injury.
