Project description:Transcriptional profiling of zebrafish embryo comparing wild type untreated embryos with embryos injected with morpholino of zf-bad. This assay is used for determination of expression profiling at 24 hpf and 48 hpf under Bad deficiency. Two-condition experiment, wild type vs. MO-Bad treated cells. Biological replicates: each group contains 200 embryos.

2014-06-01 | E-GEOD-47971 | biostudies-arrayexpress

Mouse Mammary Gland Morphogenic Differences with BAD 3SA Mutant

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.

2021-03-29 | PXD014347 | Pride

The RhoJ-BAD Signaling Network: An Achilles Heel for BRAF Mutant Melanomas

Project description:Genes and pathways that allow cells to cope with oncogene-induced stress represent selective cancer therapeutic targets that remain largely undiscovered. In this study, we identify a RhoJ signaling pathway that is a selective therapeutic target for BRAF mutant cells. RhoJ deletion in BRAF mutant melanocytes modulates the expression of the pro-apoptotic protein BAD as well as genes involved in cellular metabolism, impairing nevus formation, cellular transformation, and metastasis. Short-term treatment of nascent melanoma tumors with PAK inhibitors that block RhoJ signaling halts the growth of BRAF mutant melanoma tumors in vivo and induces apoptosis in melanoma cells in vitro via a BAD-dependent mechanism. As up to 50% of BRAF mutant human melanomas express high levels of RhoJ, these studies nominate the RhoJ-BAD signaling network as a therapeutic vulnerability for fledgling BRAF mutant human tumors.

2017-07-26 | GSE101859 | GEO

Massilia chloroacetimidivorans strain:TA-C7e

Project description:Genome sequencing and assembly of herbicide-degrading bacterium

| PRJNA353546 | ENA