Project description:We used microarrays to detail genome-wide gene expression underlying cardiac myocyte pathologies and identified candidate genes and specific pathways affecting cardiac myopathies Keywords: transgenics, cardiac disease analysis Mouse heart atria were dissected for RNA extraction and hybridisation on Affymetrix microarrays. We sought to profile gene expression from the transgenic mouse models for non-transgenics (Ntg), dnPI3K (dominant negative for phosphoinositide 3-kinase), Mst1 (mammalian sterile 20-like kinase 1) and dnPI3K-Mst1 (double mutant) mouse models with a combined background of C57BL/6/FVB/N inbred strains. Pathological insults on cardiac myocytes are investigated
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from Mus musculus tissues (Heart, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from seven Mus musculus tissues (Heart, Brain, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from Mus musculus tissues (Heart, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from seven Mus musculus tissues (Heart, Brain, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
Project description:Here, we undertook comprehensive physiological and molecular analyses in cardiac-specific transgenic mice with increased or decreased PI3K to assess the dose response impact of directly regulating PI3K. Elevated PI3K was associated with a dose-dependent increase in heart size, and preserved/enhanced function. In contrast, reduced PI3K led to cardiac dysfunction, fibrosis, arrhythmia, and increased susceptibility to atrial enlargement and thrombi. This phenotype was associated with dysregulation of a lipid species (GM3) that regulates the IGF1-PI3K pathway, cardiac stress and contractility genes. Proteomic profiling identified distinct signatures across atria with varying degrees of atrial dysfunction, enlargement, and presence of atrial thrombi.
