Emily Omori

Works (10)

Updated: July 6th, 2023 21:13

2016 article

TAK1 regulates hepatic lipid homeostasis through SREBP

Morioka, S., Sai, K., Omori, E., Ikeda, Y., Matsumoto, K., & Ninomiya-Tsuji, J. (2016, March 14). Oncogene, Vol. 35, pp. 3829–3838.

By: S. Morioka n, K. Sai n, E. Omori n, Y. Ikeda  n, K. Matsumoto * & J. Ninomiya-Tsuji n 

Contributors: S. Morioka n, K. Sai n, E. Omori 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
topics (OpenAlex): Cholesterol and Lipid Metabolism; Peroxisome Proliferator-Activated Receptors; Drug Transport and Resistance Mechanisms
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)
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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

2014 journal article

TAK1 kinase switches cell fate from apoptosis to necrosis following TNF stimulation

Journal of Cell Biology, 204(4), 607–623.

By: S. Morioka, P. Broglie, E. Omori, Y. Ikeda, G. Takaesu, K. Matsumoto, J. Ninomiya-Tsuji

Source: NC State University Libraries
Added: August 6, 2018

2011 article

Non-canonical β-catenin degradation mediates reactive oxygen species-induced epidermal cell death

Omori, E., Matsumoto, K., & Ninomiya-Tsuji, J. (2011, March 7). Oncogene, Vol. 30, pp. 3336–3344.

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

Contributors: E. Omori 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
topics (OpenAlex): Ubiquitin and proteasome pathways; Cancer-related gene regulation
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)
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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.

By: R. Kajino-Sakamoto  n, E. Omori n, P. Nighot n, A. Blikslager n , K. Matsumoto * & J. Ninomiya-Tsuji n 

Contributors: R. Kajino-Sakamoto  n, E. Omori 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
topics (OpenAlex): Helicobacter pylori-related gastroenterology studies; Genomics, phytochemicals, and oxidative stress
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)
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Sources: Web Of Science, Crossref, ORCID, NC State University Libraries
Added: August 6, 2018

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

2009 article

TAK1 kinase determines TRAIL sensitivity by modulating reactive oxygen species and cIAP

Morioka, S., Omori, E., Kajino, T., Kajino-Sakamoto, R., Matsumoto, K., & Ninomiya-Tsuji, J. (2009, May 4). Oncogene, Vol. 28, pp. 2257–2265.

By: S. Morioka*, E. Omori n, T. Kajino *, R. Kajino-Sakamoto n, K. Matsumoto * & J. Ninomiya-Tsuji n 

Contributors: S. Morioka*, E. Omori 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
topics (OpenAlex): Cell death mechanisms and regulation; Immune Response and Inflammation
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)
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Sources: Web Of Science, NC State University Libraries, ORCID
Added: August 6, 2018

2008 article

TAK1 Regulates Reactive Oxygen Species and Cell Death in Keratinocytes, Which Is Essential for Skin Integrity

Omori, E., Morioka, S., Matsumoto, K., & Ninomiya-Tsuji, J. (2008, July 8). Journal of Biological Chemistry, Vol. 283, pp. 26161–26168.

By: E. Omori n, S. Morioka  n, K. Matsumoto * & J. Ninomiya-Tsuji n 

Contributors: E. Omori 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
topics (OpenAlex): Immune Response and Inflammation; interferon and immune responses
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)
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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

2007 article

TAK1 MAPK Kinase Kinase Mediates Transforming Growth Factor-β Signaling by Targeting SnoN Oncoprotein for Degradation

Kajino, T., Omori, E., Ishii, S., Matsumoto, K., & Ninomiya-Tsuji, J. (2007, February 4). Journal of Biological Chemistry, Vol. 282, pp. 9475–9481.

By: T. Kajino *, E. Omori n, S. Ishii, K. Matsumoto * & J. Ninomiya-Tsuji n 

Contributors: T. Kajino *, E. Omori 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
topics (OpenAlex): Bone Metabolism and Diseases
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)
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UN Sustainable Development Goal Categories
Sources: Web Of Science, NC State University Libraries, ORCID
Added: August 6, 2018

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