Jae-Young Kim

MeSH headings : Animals; Apoptosis; Cell Proliferation; Colitis / chemically induced; Colitis / etiology; Cyclooxygenase 2; Dextran Sulfate; Interleukin-6; Intestinal Mucosa / metabolism; MAP Kinase Kinase Kinases / deficiency; MAP Kinase Kinase Kinases / physiology; Mice; Mice, Knockout; Receptors, Tumor Necrosis Factor, Type I / deficiency; Signal Transduction

TL;DR: It is shown that TAK1 is essential for interleukin 1- and bacterial components-induced expression of cytoprotective factors and cell proliferation, which is pivotal for protecting the intestinal epithelium against injury. (via Semantic Scholar)

MeSH headings : Adaptor Proteins, Signal Transducing / genetics; Adaptor Proteins, Signal Transducing / metabolism; Animals; Cell Line; Cytokines / metabolism; Embryo, Mammalian / cytology; Embryo, Mammalian / metabolism; Enzyme Activation / physiology; Fibroblasts / cytology; Fibroblasts / metabolism; MAP Kinase Kinase Kinases / genetics; MAP Kinase Kinase Kinases / metabolism; Mice; Mice, Knockout; Osmotic Pressure / physiology; Protein Structure, Tertiary / physiology; Signal Transduction / physiology

TL;DR: It is found that TAK1 is spontaneously activated when the concentration is increased and that it is totally dependent on TAB1, and that the C-terminal 68 amino acids of TAB 1 were sufficient to mediate osmotic stress-induced TAK 1 activation. (via Semantic Scholar)

MeSH headings : Acetylmuramyl-Alanyl-Isoglutamine / pharmacology; Animals; Cell Line; Cell Line, Tumor; Cells, Cultured; Chemokines, CXC / genetics; Chemokines, CXC / metabolism; Electrophoretic Mobility Shift Assay; Humans; Immunity, Innate / drug effects; Immunoblotting; Immunoprecipitation; JNK Mitogen-Activated Protein Kinases / genetics; JNK Mitogen-Activated Protein Kinases / metabolism; Keratinocytes / cytology; Keratinocytes / drug effects; Keratinocytes / metabolism; MAP Kinase Kinase Kinases / genetics; MAP Kinase Kinase Kinases / metabolism; Mice; Mice, Mutant Strains; Models, Biological; NF-kappa B / genetics; NF-kappa B / metabolism; Nod2 Signaling Adaptor Protein / genetics; Nod2 Signaling Adaptor Protein / metabolism; Receptor-Interacting Protein Serine-Threonine Kinase 2 / genetics; Receptor-Interacting Protein Serine-Threonine Kinase 2 / metabolism; Reverse Transcriptase Polymerase Chain Reaction; Signal Transduction / drug effects; Transfection; Tumor Necrosis Factor-alpha / genetics; Tumor Necrosis Factor-alpha / metabolism; p38 Mitogen-Activated Protein Kinases / metabolism

TL;DR: It is shown that transforming growth factor β-activated kinase 1 (TAK1) is an essential intermediate of NOD2 signaling and its ablation may impair the skin barrier function leading to inflammation. (via Semantic Scholar)