Project description:This study was performed to identify transcripts that are differentially expressed in the mammary gland at 4 stages of developmental (virgin, pregnant, lactating and involution) in wild type C57BL/6J mice. Keywords: developmental stage
Project description:The identification of genes driving organ development is central to understanding which signaling pathways drive the pathogenesis of various diseases including cancer. This dataset depicts the proteomic changes observed in C57BL/6J mice expressing wild-type or 3SA-phospho mutant versions of the Bcl-2-associated death promoter, BAD. This data shows that BAD regulates postnatal mammary gland morphogenesis in puberty. Three conserved serine residues on BAD are co-ordinately phosphorylated to regulate its activity. Non-phosphorylated BAD mutant delayed pubertal ductal elongation. This defect was specific to the epithelial compartment as transplant and ex vivo organoid assays of mutant epithelium recapitulated decreased tubule migration. Proteomic signature between BAD+/+ and phosphomutant BAD-3SA mammary glands identified differences in actin-binding and focal adhesion components. Mechanistically, non-phosphorylated BAD impedes protein translation, specifically in protrusions, through aberrant hypophosphorylated 4E-BP1. These findings reveal a critical enhancement of localized translation for efficient pubertal-mammary-gland morphogenesis and identifies BAD as a novel regulator of this process.
Project description:This study was performed to identify transcripts that are differentially expressed in the mammary gland at 4 stages of developmental (virgin, pregnant, lactating and involution) in wild type C57BL/6J mice. Experiment Overall Design: Whole mammary glands No4 (inguinal) were obtained from female mice at 4 stages of development: Virgin (puberty, 6 wks of age), Pregnant (14 days of pregnancy), Lactating (day 10 postpartum) and Involution (4 days post weaning of pups). Three biological replicates were obtained from Virgin females and two biological replicates for the three other stages. mice
Project description:Whole lenses were dissected from E15.5, P1, or P30 wild-type C57BL/6J mice or from K6W-Ub transgenic mice, which develop congenital cataracts. Lens homogenates were subjected to quantitative proteomic analysis using tandem mass tag (TMT) isobaric labeling.
Project description:Mammary gland aging is due to aberrant activation of p66Shc, which induces p53/p44 signaling, leading to failure of symmetric divisions, decreased proliferation and reduced regenerative potential of MaSCs. Age-related changes in mammary epithelial cells derived from C57BL/6J WT and p66Shc knockedout mice cultured as stem cell-enriched mammospheres.
