Rie Kajino-Sakamoto

author keywords: intestine; TAK1; Nrf2; Keap1; p62/SQSTM

MeSH headings : Animals; Antioxidants / metabolism; Cell Line; Gene Expression Regulation; Humans; Intestinal Mucosa / metabolism; Kelch-Like ECH-Associated Protein 1 / metabolism; MAP Kinase Kinase Kinases / genetics; MAP Kinase Kinase Kinases / metabolism; Mice; Mice, Knockout; Models, Biological; NF-E2-Related Factor 2 / genetics; NF-E2-Related Factor 2 / metabolism; Oxidative Stress; Protein Binding; Proteolysis; Reactive Oxygen Species / metabolism; Sequestosome-1 Protein / metabolism

TL;DR: The results identify for the first time that TAK1 is a modulator of p62/SQSTM1-dependent Keap1 degradation and maintains the steady state-level of Nrf2, important for homeostatic antioxidant protection in the intestinal epithelium. (via Semantic Scholar)

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)

author keywords: TAK1; TRAIL; reactive oxygen species; cIAP; apoptosis

MeSH headings : Animals; Apoptosis / drug effects; Caspase 3 / metabolism; Cell Line; Cell Line, Tumor; Cell Survival / drug effects; Electrophoretic Mobility Shift Assay; Flow Cytometry; HeLa Cells; Humans; Immunoblotting; Inhibitor of Apoptosis Proteins / metabolism; Keratinocytes / cytology; Keratinocytes / drug effects; Keratinocytes / metabolism; MAP Kinase Kinase Kinases / genetics; MAP Kinase Kinase Kinases / metabolism; Mice; Mice, Knockout; Microscopy, Fluorescence; NF-kappa B / metabolism; RNA, Small Interfering / genetics; Reactive Oxygen Species / metabolism; Recombinant Proteins / pharmacology; TNF-Related Apoptosis-Inducing Ligand / genetics; TNF-Related Apoptosis-Inducing Ligand / pharmacology; Transfection

TL;DR: It is reported that deletion of TAK1 kinase greatly increased activation of caspase-3 and cell death after TRAIL stimulation in keratinocytes, fibroblasts and cancer cells, and inhibition of Tak1 can be an effective approach to increase TRAIL sensitivity. (via Semantic Scholar)