Project description:This SuperSeries is composed of the following subset Series:; GSE10726: Expression data from skin of epithelial activated beta-catenin mutant mouse embryo; GSE10727: Expression data from dermis of epithelial activated beta-catenin mutant mouse embryo; GSE10728: Expression data from epidermis of epithelial activated beta-catenin mutant mouse embryo Experiment Overall Design: Refer to individual Series
Project description:Forced expression of activated beta-catenin in mouse dermal fibroblasts is sufficient to cause spontaneous, progressive skin fibrosis in vivo. We generated triple-transgenic HoxB6CreERT/+; R26-YFP/+; CatnbΔex3/+ "activated beta-catenin" mice and double-transgenic HoxB6CreERT/+; R26-YFP/+ littermate control mice. We induced Cre activity (resulting in expression of activated beta-catenin in triple-transgenic mutant fetuses) by administering tamoxifen to the pregnant dam at embryonic day 16.5. The activated beta-catenin mice developed fibrotic skin, characterized by elevated collagen deposition and increased fibroblast proliferation. We performed RNA-sequencing to profile gene expression in the dermis of control and activated beta-catenin mutant mice with established skin fibrosis at 3 weeks of age.
Project description:In nucleated cells, β-catenin, the key downstream effector of this pathway, is a dual function protein, regulating the coordination of gene transcription and cell–cell adhesion. The specific role of β-catenin in the anucleate platelet however remains elusive. Here, we performed a label-free quantitative proteomic analysis of β-catenin immunoprecipitates from human platelets identifying 9 co-immunoprecipitating proteins. GO biological pathway analysis revealed a significant enrichment of specific functional terms including 'cell adhesion', 'cell junction organization' and ‘adherens junction organization'. Our bioinformatics data suggests that human platelet β-catenin may be involved in facilitating cell adhesion and cell junctions. We found three proteins co-immunoprecipitating with β-catenin under both resting and activated conditions, four proteins under resting condition only and two proteins under activated condition only.
Project description:Hepatoblastoma (HB), the most common type of pediatric liver cancer, is associated with aberrant wnt/β-catenin activation and Myc amplification/overexpression. Mice expressing both alleles developed HBs and HCCs with incomplete penetrance by 5-6 weeks of age with fetal and mixed fetal/embryonal HBs, the most prevalent histologic HB subtypes seen in children being the predominant tumor types. To address the roles of mutant wnt/β-catenin activation and Myc over-expression in the pathogenesis of HB, c-Myc and mutant dominant-stable β-catenin were co-targeted to immature cells of the developing mouse liver.
Project description:We generated a murine genetic model of beta-catenin deficiency targeted to the ureteric bud cell lineage to study the role of beta-catenin mediated Wnt signaling during ureteric morphogenesis. Experiment Overall Design: A comparison was made between triplicate samples of E12.5 kidneys from either normal mice or mice with a b-catenin allele containing LoxP sites flanking exons 2 through 6 crossed to Hoxb7-Cre:Gfp mice
