Jae-Young Kim

Works (3)

Updated: July 5th, 2023 15:54

2009 article

Intestinal Epithelial-Derived TAK1 Signaling Is Essential for Cytoprotection against Chemical-Induced Colitis

Kim, J.-Y., Kajino-Sakamoto, R., Omori, E., Jobin, C., & Ninomiya-Tsuji, J. (2009, February 20). PLoS ONE, Vol. 4.

By: J. Kim n, R. Kajino-Sakamoto n, E. Omori n, C. Jobin * & J. Ninomiya-Tsuji n 

Contributors: J. Kim n, R. Kajino-Sakamoto n, E. Omori n, C. Jobin * & J. Ninomiya-Tsuji n 

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
topics (OpenAlex): Immune Response and Inflammation; Helicobacter pylori-related gastroenterology studies
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)
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3. Good Health and Well-being (Web of Science; OpenAlex)
Sources: Web Of Science, NC State University Libraries, ORCID
Added: August 6, 2018

2008 article

TAK1-binding Protein 1, TAB1, Mediates Osmotic Stress-induced TAK1 Activation but Is Dispensable for TAK1-mediated Cytokine Signaling

Inagaki, M., Omori, E., Kim, J.-Y., Komatsu, Y., Scott, G., Ray, M. K., … Ninomiya-Tsuji, J. (2008, October 2). Journal of Biological Chemistry, Vol. 283, pp. 33080–33086.

By: M. Inagaki n, E. Omori n, J. Kim n, Y. Komatsu *, G. Scott*, M. Ray*, . Yamada *, K. Matsumoto *, Y. Mishina *, J. Ninomiya-Tsuji n 

Contributors: M. Inagaki n, E. Omori n, J. Kim n, Y. Komatsu *, G. Scott*, M. Ray*, G. Yamada *, K. Matsumoto *, Y. Mishina *, J. Ninomiya-Tsuji n 

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
topics (OpenAlex): Immune Response and Inflammation; Neutrophil, Myeloperoxidase and Oxidative Mechanisms
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)
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Sources: Web Of Science, NC State University Libraries, ORCID
Added: August 6, 2018

2007 article

TAK1 Is a Central Mediator of NOD2 Signaling in Epidermal Cells

Kim, J.-Y., Omori, E., Matsumoto, K., Núñez, G., & Ninomiya-Tsuji, J. (2007, October 26). Journal of Biological Chemistry, Vol. 283, pp. 137–144.

By: J. Kim n, E. Omori n, K. Matsumoto *, G. Núñez * & J. Ninomiya-Tsuji n 

Contributors: J. Kim n, E. Omori n, K. Matsumoto *, G. Núñez * & J. Ninomiya-Tsuji n 

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
topics (OpenAlex): Immune Response and Inflammation; Cell Adhesion Molecules Research
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)
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Sources: Web Of Science, NC State University Libraries, ORCID
Added: August 6, 2018

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