Emily Omori
Works (10)
Updated: July 6th, 2023 21:13
2016 journal article
TAK1 regulates hepatic lipid homeostasis through SREBP
ONCOGENE, 35(29), 3829–3838.
Contributors: S. Morioka n, K. Sai n, n, Y. Ikeda n, K. Matsumoto * & J. Ninomiya-Tsuji n
MeSH headings : Animals; Carcinoma, Hepatocellular / genetics; Carcinoma, Hepatocellular / metabolism; Cell Line; Fatty Liver / genetics; Fatty Liver / metabolism; Female; HEK293 Cells; Hep G2 Cells; Hepatocytes / metabolism; Homeostasis; Humans; Immunoblotting; Lipid Metabolism; Liver / metabolism; Liver Neoplasms / genetics; Liver Neoplasms / metabolism; MAP Kinase Kinase Kinases / genetics; MAP Kinase Kinase Kinases / metabolism; Male; Mice, Inbred C57BL; Mice, Knockout; Mice, Transgenic; Protein Binding; RNA Interference; Risk Factors; Sterol Regulatory Element Binding Proteins / genetics; Sterol Regulatory Element Binding Proteins / metabolism
TL;DR:
It is demonstrated that SREBPs are regulated by a previously uncharacterized mechanism through transforming growth factor-β activated kinase 1 (TAK1), a signaling molecule of inflammation, which critically contributes to the maintenance of liver homeostasis to prevent steatosis.
(via Semantic Scholar)
open access via europepmc.org (repository)
UN Sustainable Development Goal Categories
3. Good Health and Well-being
(Web of Science)
Sources: Web Of Science, NC State University Libraries, ORCID
Added: August 6, 2018
2014 journal article
TAK1 kinase switches cell fate from apoptosis to necrosis following TNF stimulation
Journal of Cell Biology, 204(4), 607–623.
Source: NC State University Libraries
Added: August 6, 2018
2011 journal article
Non-canonical beta-catenin degradation mediates reactive oxygen species-induced epidermal cell death
ONCOGENE, 30(30), 3336–3344.
Contributors: n, K. Matsumoto * & J. Ninomiya-Tsuji n
author keywords: apoptosis; beta-catenin; caspase; epidermis; reactive oxygen species
MeSH headings : Animals; Apoptosis / drug effects; Caspases / metabolism; Cell Adhesion / drug effects; Enzyme Activation / drug effects; Epidermal Cells; Epidermis / drug effects; Epidermis / enzymology; Epidermis / metabolism; HEK293 Cells; Humans; Mice; Reactive Oxygen Species / pharmacology; beta Catenin / metabolism
TL;DR:
Results indicate that a feed-forward loop consisting of ROS, caspases activation and β-catenin degradation induces epidermal cell death.
(via Semantic Scholar)
UN Sustainable Development Goal Categories
3. Good Health and Well-being
(Web of Science)
Sources: Web Of Science, NC State University Libraries, ORCID
Added: August 6, 2018
2010 journal article
TGF-β–Activated Kinase 1 Signaling Maintains Intestinal Integrity by Preventing Accumulation of Reactive Oxygen Species in the Intestinal Epithelium
The Journal of Immunology, 185(8), 4729–4737.
Contributors: R. Kajino-Sakamoto n, n, P. Nighot n, A. Blikslager n , K. Matsumoto * & J. Ninomiya-Tsuji n
MeSH headings : Animals; Blotting, Western; Epithelium / enzymology; Epithelium / immunology; Gene Expression; Gene Expression Regulation / immunology; Immunity, Mucosal / physiology; Immunohistochemistry; Intestinal Mucosa / enzymology; Intestinal Mucosa / immunology; MAP Kinase Kinase Kinases / immunology; MAP Kinase Kinase Kinases / metabolism; Mice; Mice, Inbred C57BL; Mice, Transgenic; NF-E2-Related Factor 2 / immunology; NF-E2-Related Factor 2 / metabolism; Oxidative Stress / immunology; Reactive Oxygen Species / immunology; Reactive Oxygen Species / metabolism; Reverse Transcriptase Polymerase Chain Reaction; Signal Transduction
TL;DR:
It is reported that TGF-β–activated kinase 1 (TAK1) is a key regulator of ROS in the intestinal epithelium and regulates ROS through transcription factor NF-E2–related factor 2, which is important for intestinal epithelial integrity.
(via Semantic Scholar)
UN Sustainable Development Goal Categories
3. Good Health and Well-being
(Web of Science)
Sources: Web Of Science, Crossref, ORCID, NC State University Libraries
Added: August 6, 2018
2009 journal article
Intestinal Epithelial-Derived TAK1 Signaling Is Essential for Cytoprotection against Chemical-Induced Colitis
PLOS ONE, 4(2).
Contributors: J. Kim n, R. Kajino-Sakamoto n, 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
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)
UN Sustainable Development Goal Categories
3. Good Health and Well-being
(Web of Science; OpenAlex)
Sources: Web Of Science, NC State University Libraries, ORCID
Added: August 6, 2018
2009 journal article
TAK1 kinase determines TRAIL sensitivity by modulating reactive oxygen species and cIAP
ONCOGENE, 28(23), 2257–2265.
Contributors: S. Morioka*, n, T. Kajino *, R. Kajino-Sakamoto n, K. Matsumoto * & J. Ninomiya-Tsuji n
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)
UN Sustainable Development Goal Categories
3. Good Health and Well-being
(Web of Science)
Sources: Web Of Science, NC State University Libraries, ORCID
Added: August 6, 2018
2008 journal article
TAK1 regulates reactive oxygen species and cell death in keratinocytes, which is essential for skin integrity
JOURNAL OF BIOLOGICAL CHEMISTRY, 283(38), 26161–26168.
Contributors: n, S. Morioka n, K. Matsumoto * & J. Ninomiya-Tsuji n
MeSH headings : Animals; Antioxidants / metabolism; Cytochromes c / metabolism; Gene Expression Regulation; Inflammation; Keratinocytes / cytology; Keratinocytes / metabolism; MAP Kinase Kinase Kinases / metabolism; Mice; Mice, Transgenic; Models, Biological; NF-kappa B / metabolism; Oxidative Stress; Proto-Oncogene Proteins c-jun / metabolism; Reactive Oxygen Species; Skin / metabolism
TL;DR:
It is shown that, in an in vivo setting, the antioxidant treatment could reduce an inflammatory condition in keratinocyte-specific Tak1 deletion mice and regulate ROS partially through c-Jun, which is important for preventing ROS-induced skin inflammation.
(via Semantic Scholar)
UN Sustainable Development Goal Categories
3. Good Health and Well-being
(Web of Science)
Sources: Web Of Science, NC State University Libraries, ORCID
Added: August 6, 2018
2008 journal article
TAK1-binding Protein 1, TAB1, Mediates Osmotic Stress-induced TAK1 Activation but Is Dispensable for TAK1-mediated Cytokine Signaling
JOURNAL OF BIOLOGICAL CHEMISTRY, 283(48), 33080–33086.
Contributors: M. Inagaki n, 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
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)
UN Sustainable Development Goal Categories
3. Good Health and Well-being
(Web of Science)
Sources: Web Of Science, NC State University Libraries, ORCID
Added: August 6, 2018
2007 journal article
TAK1 MAPK kinase kinase mediates transforming growth factor-beta signaling by targeting SnoN oncoprotein for degradation
JOURNAL OF BIOLOGICAL CHEMISTRY, 282(13), 9475–9481.
Contributors: T. Kajino *, n, S. Ishii, K. Matsumoto * & J. Ninomiya-Tsuji n
MeSH headings : Cell Line, Transformed; HeLa Cells; Humans; Intracellular Signaling Peptides and Proteins / metabolism; MAP Kinase Kinase Kinases / physiology; Phosphorylation; Proto-Oncogene Proteins / metabolism; Signal Transduction / physiology; Transforming Growth Factor beta / physiology
TL;DR:
The data suggest that TAK1 modulates TGF-β-dependent cellular responses by targeting SnoN for degradation, and this phosphorylation regulated the stability of SnoN.
(via Semantic Scholar)
UN Sustainable Development Goal Categories
3. Good Health and Well-being
(Web of Science)
Sources: Web Of Science, NC State University Libraries, ORCID
Added: August 6, 2018
2007 journal article
TAK1 is a central mediator of NOD2 signaling in epidermal cells
JOURNAL OF BIOLOGICAL CHEMISTRY, 283(1), 137–144.
Contributors: J. Kim 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
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)
UN Sustainable Development Goal Categories
3. Good Health and Well-being
(Web of Science)
Sources: Web Of Science, NC State University Libraries, ORCID
Added: August 6, 2018
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