Works (57)

Updated: April 3rd, 2024 17:48

2023 journal article

Aberrantly activated TAK1 links neuroinflammation and neuronal loss in Alzheimer?s disease mouse models

JOURNAL OF CELL SCIENCE, 136(6).

By: K. Sai n, A. Nakanishi n, K. Scofield n, D. Tokarz n, K. Linder n, T. Cohen*, J. Ninomiya-Tsuji n

author keywords: Alzheimer?s disease; Cell death; Inflammation; TAK1
MeSH headings : Animals; Mice; Alzheimer Disease / genetics; Calcium; Cytokines / metabolism; Neuroinflammatory Diseases; Signal Transduction / physiology
TL;DR: It is reported that compound stimulation with the neurotoxic factors TNF and glutamate aberrantly activates neuronal TAK1 (also known as MAP3K7), which promotes the pathogenesis of AD in mouse models and provides a molecular mechanism linking cytokines, Ca2+ signaling and neuronal necroptosis in AD. (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: May 30, 2023

2021 journal article

TAK1 inhibition elicits mitochondrial ROS to block intracellular bacterial colonization

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 118(25).

By: W. Lopez-Perez n, K. Sai n, Y. Sakamachi n, C. Parsons n, S. Kathariou n & J. Ninomiya-Tsuji n

author keywords: TAK1; ROS; mitochondria; intracellular bacteria
MeSH headings : Animals; Bacteria / growth & development; Caspase 3 / metabolism; Colony Count, Microbial; Hydrogen Sulfide / pharmacology; Intracellular Space / microbiology; MAP Kinase Kinase Kinases / antagonists & inhibitors; MAP Kinase Kinase Kinases / metabolism; Mice; Mitochondria / metabolism; Reactive Oxygen Species / metabolism; Receptor-Interacting Protein Serine-Threonine Kinases / metabolism; Salmonella / drug effects; Salmonella / growth & development; Yersinia / drug effects
TL;DR: A previously unrecognized host defense mechanism is revealed, which is initiated by host recognition of pathogen-induced impairment in a host protein, TAK1, but not directly of pathogens. (via Semantic Scholar)
UN Sustainable Development Goal Categories
Source: Web Of Science
Added: July 12, 2021

2019 journal article

Coordinating Tissue Regeneration Through Transforming Growth Factor-beta Activated Kinase 1 Inactivation and Reactivation

STEM CELLS, 37(6), 766–778.

By: H. Hsieh*, S. Agarwal*, D. Cholok*, S. Loder*, K. Kaneko*, A. Huber*, M. Chung*, K. Ranganathan* ...

author keywords: Cellular proliferation; Differentiation; Progenitor cells; Proliferation; Stem; progenitor cell; Tissue regeneration
MeSH headings : Animals; Bone Regeneration / drug effects; Bone Regeneration / genetics; Cell Differentiation / drug effects; Cell Proliferation / drug effects; DNA Nucleotidyltransferases / genetics; DNA Nucleotidyltransferases / metabolism; Female; Founder Effect; Fractures, Bone / drug therapy; Fractures, Bone / enzymology; Fractures, Bone / genetics; Fractures, Bone / pathology; Gene Expression Regulation; Integrases / genetics; Integrases / metabolism; MAP Kinase Kinase Kinases / antagonists & inhibitors; MAP Kinase Kinase Kinases / deficiency; MAP Kinase Kinase Kinases / genetics; Male; Mesenchymal Stem Cells / cytology; Mesenchymal Stem Cells / drug effects; Mesenchymal Stem Cells / enzymology; Mice; Mice, Inbred C57BL; Mice, Transgenic; Osteoblasts / cytology; Osteoblasts / drug effects; Osteoblasts / enzymology; Primary Cell Culture; Protein Kinase Inhibitors / pharmacology; Signal Transduction; Skull / drug effects; Skull / injuries; Skull / metabolism; Wound Healing / drug effects; Wound Healing / genetics
TL;DR: It is demonstrated that loss of transforming growth factor‐β activated kinase 1 (TAK1) signaling reduces inappropriate tissue formation (heterotopic ossification) through reduced cellular differentiation, and the importance of both the “drug on” and "drug off" states during regenerative therapy is revealed. (via Semantic Scholar)
UN Sustainable Development Goal Categories
3. Good Health and Well-being (Web of Science; OpenAlex)
Source: Web Of Science
Added: July 22, 2019

2019 journal article

Necroptosis mediators RIPK3 and MLKL suppress intracellular Listeria replication independently of host cell killing

JOURNAL OF CELL BIOLOGY, 218(6), 1994–2005.

By: K. Sai n, C. Parsons n, J. House n, S. Kathariou n & J. Ninomiya-Tsuji n

Contributors: K. Sai n, C. Parsons n, J. House n, S. Kathariou n & J. Ninomiya-Tsuji n

MeSH headings : Animals; Female; Humans; Listeria / growth & development; Listeria / immunology; Listeria / metabolism; Listeriosis / metabolism; Listeriosis / microbiology; Listeriosis / pathology; Listeriosis / prevention & control; Mice; Mice, Inbred C57BL; Mice, Knockout; Necroptosis; Protein Kinases / physiology; Receptor-Interacting Protein Serine-Threonine Kinases / genetics; Receptor-Interacting Protein Serine-Threonine Kinases / metabolism; Receptor-Interacting Protein Serine-Threonine Kinases / physiology
TL;DR: The RIPK3-MLKL pathway protects epithelial cells from Listeria monocytogenes invasion but does not induce its oligomerization or necroptotic cell death, and instead targets intracellular bacteria and suppresses their replication. (via Semantic Scholar)
Sources: Web Of Science, ORCID, NC State University Libraries
Added: June 24, 2019

2018 journal article

Compound mutations in Bmpr1a and Tak1 synergize facial deformities via increased cell death

GENESIS, 56(3).

By: X. Liu*, S. Hayano*, H. Pan*, M. Inagaki n, J. Ninomiya-Tsuji n, H. Sun*, Y. Mishina*

author keywords: apoptosis; facial prominence; MAP kinase; nasal septum; Smad signaling
MeSH headings : Animals; Apoptosis / genetics; Biomarkers; Bone Morphogenetic Protein Receptors, Type I / genetics; Bone Morphogenetic Protein Receptors, Type I / metabolism; Cell Death / genetics; Craniofacial Abnormalities / diagnosis; Craniofacial Abnormalities / genetics; Genetic Association Studies; Genotype; Gestational Age; Immunohistochemistry; MAP Kinase Kinase Kinases / genetics; MAP Kinase Kinase Kinases / metabolism; Mice; Mice, Transgenic; Mutation; Phenotype; Signal Transduction; Smad Proteins / metabolism; p38 Mitogen-Activated Protein Kinases / metabolism
TL;DR: It is suggested that deletion of Tak1 aggravates the craniofacial deformities of the caBmpr1a mutants by increasing p53 and phospho‐p38 at different stage of embryogenesis. (via Semantic Scholar)
UN Sustainable Development Goal Categories
3. Good Health and Well-being (Web of Science; OpenAlex)
Source: Web Of Science
Added: August 6, 2018

2017 journal article

Erratum: Noncanonical cell death program independent of caspase activation cascade and necroptotic modules is elicited by loss of TGFβ-activated kinase 1

Scientific Reports, 7(1).

By: S. Mihaly n, Y. Sakamachi n, J. Ninomiya-Tsuji n & S. Morioka n

Source: Crossref
Added: August 28, 2020

2017 journal article

Noncanocial cell death program independent of caspase activation cascade and necroptotic modules is elicited by loss of TGF beta-activated kinase 1

SCIENTIFIC REPORTS, 7.

By: S. Mihaly n, Y. Sakamachi n, J. Ninomiya-Tsuji n & S. Morioka n

TL;DR: This work identified a previously uncharacterized cell death pathway regulated by TAK1, which is unexpectedly provoked by inhibition of caspase activity and necroptosis cascades and surprisingly found that caspases and RIPK3 inhibitions do not completely suppress cell death in Tak1-deficient cells. (via Semantic Scholar)
Source: Web Of Science
Added: August 6, 2018

2017 journal article

TAK1 regulates resident macrophages by protecting lysosomal integrity

CELL DEATH & DISEASE, 8.

By: Y. Sakamachi n, S. Morioka n, S. Mihaly n, G. Takaesu n, J. Foley*, M. Fessler*, J. Ninomiya-Tsuji n

MeSH headings : Animals; Cell Death / physiology; Cell Survival / physiology; Embryonic Development / physiology; Lung / metabolism; Lysosomes / metabolism; MAP Kinase Kinase Kinases / metabolism; Macrophages / metabolism; Mice; Mice, Inbred C57BL; Protective Agents / metabolism; Receptors, Tumor Necrosis Factor, Type I / metabolism; Signal Transduction / physiology; Thymocytes / physiology; Thymus Gland / metabolism; Toll-Like Receptors / metabolism
TL;DR: The results suggest that autocrine and potentially paracrine TNF kills Tak1-deficient macrophages during development, and reveal that TAK1 signaling maintains proper macrophage populations through protecting lysosomal integrity. (via Semantic Scholar)
UN Sustainable Development Goal Categories
3. Good Health and Well-being (Web of Science; OpenAlex)
Source: Web Of Science
Added: August 6, 2018

2016 journal article

TAK1 Regulates the Nrf2 Antioxidant System Through Modulating p62/SQSTM1

ANTIOXIDANTS & REDOX SIGNALING, 25(17), 953–964.

By: K. Hashimoto n, A. Simmons*, R. Kajino-Sakamoto*, Y. Tsuji n & J. Ninomiya-Tsuji n

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)
Source: Web Of Science
Added: August 6, 2018

2016 journal article

TAK1 determines susceptibility to endoplasmic reticulum stress and leptin resistance in the hypothalamus

Journal of Cell Science, 129(9), 1855–1865.

author keywords: TAK1; Endoplasmic reticulum stress; Leptin; Hypothalamus; Obesity
MeSH headings : Animals; Dietary Fats / adverse effects; Dietary Fats / pharmacology; Endoplasmic Reticulum Stress; Hyperphagia / chemically induced; Hyperphagia / genetics; Hyperphagia / metabolism; Hyperphagia / pathology; Hypothalamus / metabolism; Hypothalamus / pathology; Leptin / genetics; Leptin / metabolism; MAP Kinase Kinase Kinases / genetics; MAP Kinase Kinase Kinases / metabolism; Mice; Mice, Knockout; Obesity / chemically induced; Obesity / genetics; Obesity / metabolism; Obesity / pathology; Sterol Regulatory Element Binding Proteins / genetics; Sterol Regulatory Element Binding Proteins / metabolism
TL;DR: It is found that deletion of Tak1 increased ER volume and facilitated ER-stress tolerance in cultured cells, which was mediated by upregulation of sterol-regulatory-element-binding protein (SREBP)-dependent lipogenesis and central nervous system (CNS) deletion upregulated SREBP-target lipogenic genes and blocked ER stress in the hypothalamus. (via Semantic Scholar)
UN Sustainable Development Goal Categories
3. Good Health and Well-being (Web of Science; OpenAlex)
Sources: Web Of Science, Crossref
Added: August 6, 2018

2016 journal article

TAK1 regulates Paneth cell integrity partly through blocking necroptosis

CELL DEATH & DISEASE, 7.

By: A. Simmons n, R. Kajino-Sakamoto n & J. Ninomiya-Tsuji n

MeSH headings : Animals; Anti-Bacterial Agents / pharmacology; Apoptosis / drug effects; Bacteria / drug effects; Bacteria / genetics; DNA, Bacterial / genetics; DNA, Bacterial / metabolism; Intestinal Mucosa / metabolism; Intestines / microbiology; Intestines / pathology; MAP Kinase Kinase Kinases / genetics; MAP Kinase Kinase Kinases / metabolism; Mice; Mice, Inbred C57BL; Mice, Knockout; Myeloid Differentiation Factor 88 / deficiency; Myeloid Differentiation Factor 88 / genetics; Myeloid Differentiation Factor 88 / metabolism; Necrosis; Paneth Cells / drug effects; Paneth Cells / metabolism; Paneth Cells / pathology; RNA, Messenger / metabolism; Reactive Oxygen Species / metabolism; Real-Time Polymerase Chain Reaction; Receptor-Interacting Protein Serine-Threonine Kinases / genetics; Receptor-Interacting Protein Serine-Threonine Kinases / metabolism; Signal Transduction; Toll-Like Receptors / metabolism; Up-Regulation
TL;DR: It is found that depletion of gut bacteria or myeloid differentiation factor 88 (Myd88), a mediator of bacteria-derived cell signaling, reduced ROS but did not block Paneth cell loss, suggesting that gut bacteria are the cause of ROS accumulation but bacteria-induced ROS are not the cause. (via Semantic Scholar)
Source: Web Of Science
Added: August 6, 2018

2016 journal article

TAK1 regulates hepatic lipid homeostasis through SREBP

ONCOGENE, 35(29), 3829–3838.

By: 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
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)
Source: Web Of Science
Added: August 6, 2018

2015 journal article

Tak1, Smad4 and Trim33 redundantly mediate TGF-beta 3 signaling during palate development

DEVELOPMENTAL BIOLOGY, 398(2), 231–241.

By: J. Lane*, K. Yumoto*, M. Azhar*, J. Ninomiya-Tsuji n, M. Inagaki n, Y. Hu*, C. Deng*, J. Kim*, Y. Mishina*, V. Kaartinen*

author keywords: TGF-beta 3 signaling; Palatogenesis; Tak1; Smad4; Trim33
MeSH headings : Animals; Apoptosis / genetics; Cell Fusion; Cell Proliferation; Crosses, Genetic; Embryo, Mammalian / metabolism; Enzyme Activation; Epithelial Cells / metabolism; Epithelium / metabolism; Female; Gene Deletion; Gene Expression Regulation, Developmental; MAP Kinase Kinase Kinases / metabolism; Male; Matrix Metalloproteinase 13 / metabolism; Mice, Knockout; Models, Biological; Mutation / genetics; Organ Specificity; Palate / abnormalities; Palate / embryology; Palate / enzymology; Palate / metabolism; Signal Transduction; Smad4 Protein / metabolism; Transcription Factors / metabolism; Transforming Growth Factor beta3 / metabolism
TL;DR: The data reveal added complexity in TGF-β signaling during palatogenesis and demonstrate that functionally redundant pathways involving Smad4, Tak1 and Trim33 regulate palatal epithelial fusion. (via Semantic Scholar)
Source: Web Of Science
Added: August 6, 2018

2014 journal article

Activated Macrophage Survival Is Coordinated by TAK1 Binding Proteins

PLOS ONE, 9(4).

By: S. Mihaly n, S. Morioka n, J. Ninomiya-Tsuji n & G. Takaesu n

MeSH headings : Adaptor Proteins, Signal Transducing / genetics; Adaptor Proteins, Signal Transducing / metabolism; Animals; Cell Death / drug effects; Cell Death / immunology; Cell Survival / genetics; GTPase-Activating Proteins / antagonists & inhibitors; GTPase-Activating Proteins / genetics; GTPase-Activating Proteins / metabolism; Gene Deletion; Lipopolysaccharides / immunology; MAP Kinase Kinase Kinases / genetics; Macrophage Activation / genetics; Macrophage Activation / immunology; Macrophages / immunology; Macrophages / metabolism; Mice; Mice, Knockout
TL;DR: It is reported that TGFβ- activated kinase (TAK1) activators, TAK1-binding protein 1 (TAB1) and TAK2, are critical molecules in the regulation of activated macrophage survival, and shows that TAB1 and TAB2 were redundantly involved in LPS-induced Taker1 activation in macrophages. (via Semantic Scholar)
Source: Web Of Science
Added: August 6, 2018

2014 journal article

TAK1 Binding Protein 2 Is Essential for Liver Protection from Stressors

PLOS ONE, 9(2).

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

MeSH headings : Adaptor Proteins, Signal Transducing / physiology; Alkylating Agents / toxicity; Animals; Apoptosis / drug effects; Blotting, Western; Chemical and Drug Induced Liver Injury / etiology; Chemical and Drug Induced Liver Injury / metabolism; Chemical and Drug Induced Liver Injury / prevention & control; Diethylnitrosamine / toxicity; Electrophoretic Mobility Shift Assay; Female; Hepatocytes / drug effects; Hepatocytes / metabolism; Hepatocytes / pathology; Integrases / metabolism; Lipopolysaccharides / toxicity; MAP Kinase Kinase Kinases / physiology; Male; Mice; Mice, Knockout; Mice, Transgenic; RNA, Messenger / genetics; Real-Time Polymerase Chain Reaction; Reverse Transcriptase Polymerase Chain Reaction
TL;DR: It is demonstrated that TAB2 is a sensor of stress conditions in the liver and functions to protect the liver by activating the TAK1 pathway, and a chemical stressor induced greatly exaggerated liver injury in hepatocyte-specific Tab2-deficient mice. (via Semantic Scholar)
Source: Web Of Science
Added: August 6, 2018

2014 review

TAK1 control of cell death

[Review of ]. CELL DEATH AND DIFFERENTIATION, 21(11), 1667–1676.

By: S. Mihaly n, J. Ninomiya-Tsuji n & S. Morioka n

MeSH headings : Animals; Apoptosis / physiology; Cell Death; Cell Survival; Homeostasis; Humans; MAP Kinase Kinase Kinases / metabolism; Mice; Mitogen-Activated Protein Kinases / metabolism; NF-kappa B / metabolism; Necrosis / metabolism; Signal Transduction
TL;DR: This review summarizes the consequences of TAK1 deficiency in different cell and tissue types from the perspective of cell death and also focuses on the mechanism by which Tak1 complex inhibits or promotes programmed cell death. (via Semantic Scholar)
UN Sustainable Development Goal Categories
3. Good Health and Well-being (Web of Science; OpenAlex)
Source: Web Of Science
Added: August 6, 2018

2014 journal article

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

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

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

MeSH headings : Adaptor Proteins, Signal Transducing / physiology; Animals; Apoptosis / drug effects; Blotting, Western; Cell Cycle; Chemical and Drug Induced Liver Injury / metabolism; Chemical and Drug Induced Liver Injury / pathology; Flow Cytometry; Humans; Immunoprecipitation; Integrases / metabolism; Lipopolysaccharides / toxicity; MAP Kinase Kinase Kinases / physiology; Mice; Mice, Knockout; Necrosis; Phosphorylation; RNA, Small Interfering / genetics; Receptor-Interacting Protein Serine-Threonine Kinases / antagonists & inhibitors; Receptor-Interacting Protein Serine-Threonine Kinases / physiology; Signal Transduction; Tumor Necrosis Factor-alpha / pharmacology
TL;DR: Activation of the TAK1 kinase drives RIPK3-dependent necrosis and inhibits apoptosis downstream of TNF-α stimulation. (via Semantic Scholar)
Source: Crossref
Added: February 24, 2020

2013 journal article

Kinase-Independent Feedback of the TAK1/TAB1 Complex on BCL10 Turnover and NF-kappa B Activation

MOLECULAR AND CELLULAR BIOLOGY, 33(6), 1149–1163.

By: M. Moreno-Garcia*, K. Sommer*, H. Rincon-Arano*, M. Brault*, J. Ninomiya-Tsuji n, L. Matesic*, D. Rawlings*

MeSH headings : Adaptor Proteins, Signal Transducing / metabolism; Animals; B-Lymphocytes / metabolism; CARD Signaling Adaptor Proteins / metabolism; Cell Line; Chickens; Endosomal Sorting Complexes Required for Transport / metabolism; HEK293 Cells; Humans; MAP Kinase Kinase 4 / metabolism; MAP Kinase Kinase Kinases / metabolism; Mice; Mice, Inbred C57BL; NF-kappa B / metabolism; Protein Kinase C / metabolism; Protein Kinase C beta; Proteolysis; Receptors, Antigen / metabolism; Signal Transduction; T-Lymphocytes / metabolism; Ubiquitin-Protein Ligases / metabolism; Ubiquitination
TL;DR: By directly promoting BCL10 degradation, TAK1 counterbalances NF-κB and JNK signals essential for the activation and survival of lymphocytes and CARMA1-addicted lymphoma types. (via Semantic Scholar)
Source: Web Of Science
Added: August 6, 2018

2013 journal article

TGF-beta-activated Kinase 1 (Tak1) Mediates Agonist-induced Smad Activation and Linker Region Phosphorylation in Embryonic Craniofacial Neural Crest-derived Cells

JOURNAL OF BIOLOGICAL CHEMISTRY, 288(19), 13467–13480.

By: K. Yumoto*, P. Thomas*, J. Lane*, K. Matsuzaki*, M. Inagaki n, J. Ninomiya-Tsuji n, G. Scott*, M. Ray* ...

MeSH headings : Amino Acid Motifs; Animals; Cells, Cultured; Cleft Palate / enzymology; Cleft Palate / genetics; Ectoderm / cytology; Female; Gene Expression Regulation, Developmental; Head / embryology; MAP Kinase Kinase Kinases / deficiency; MAP Kinase Kinase Kinases / genetics; MAP Kinase Kinase Kinases / physiology; Male; Mandible / abnormalities; Mice; Mice, Transgenic; Mitogen-Activated Protein Kinases / metabolism; Neural Crest / cytology; Phosphorylation; Protein Processing, Post-Translational; Protein Serine-Threonine Kinases / metabolism; Receptor, Transforming Growth Factor-beta Type I; Receptors, Transforming Growth Factor beta / metabolism; Signal Transduction; Smad Proteins / metabolism; Smad Proteins, Receptor-Regulated / metabolism; TGF-beta Superfamily Proteins / physiology; Wnt1 Protein / genetics; Wnt1 Protein / metabolism
TL;DR: It is suggested that in neural crest-derived ecto-mesenchymal cells, Tak1 provides a critical point of intersection in a complex dialogue between the canonical and noncanonical arms of TGF-β superfamily signaling required for normal craniofacial development. (via Semantic Scholar)
Source: Web Of Science
Added: August 6, 2018

2012 journal article

Epithelial transforming growth factor  -activated kinase 1 (TAK1) is activated through two independent mechanisms and regulates reactive oxygen species

Proceedings of the National Academy of Sciences, 109(9), 3365–3370.

By: E. Omori n, M. Inagaki n, Y. Mishina*, K. Matsumoto* & J. Ninomiya-Tsuji n

MeSH headings : Adaptor Proteins, Signal Transducing / deficiency; Adaptor Proteins, Signal Transducing / genetics; Adaptor Proteins, Signal Transducing / metabolism; Animals; Enzyme Activation; Epidermis / enzymology; Epithelial Cells / enzymology; Intestinal Mucosa / enzymology; Keratinocytes / enzymology; MAP Kinase Kinase Kinases / metabolism; Mice; Mice, Knockout; Oxidation-Reduction; Oxidative Stress; Phenotype; Phosphorylation; Protein Processing, Post-Translational; Reactive Oxygen Species / metabolism; Signal Transduction
TL;DR: It is demonstrated that epithelial TAK1 activity is regulated through two unique, TAB1-dependent basal and TAB2-mediated stimuli-dependent mechanisms, which are dependent on each other. (via Semantic Scholar)
Source: Crossref
Added: August 28, 2020

2012 journal article

TAK1 (MAP3K7) Signaling Regulates Hematopoietic Stem Cells through TNF-Dependent and -Independent Mechanisms

PLoS ONE, 7(11), e51073.

By: G. Takaesu*, M. Inagaki n, K. Takubo*, Y. Mishina*, P. Hess n, G. Dean n, A. Yoshimura*, K. Matsumoto* ...

Ed(s): M. Tjwa

MeSH headings : Adaptor Proteins, Signal Transducing / metabolism; Animals; Antigens, Surface / metabolism; Bone Marrow Cells / enzymology; Cell Death; Cell Proliferation; Chimerism; Hematopoietic Stem Cells / cytology; Hematopoietic Stem Cells / enzymology; Humans; MAP Kinase Kinase Kinases / deficiency; MAP Kinase Kinase Kinases / metabolism; MAP Kinase Signaling System; Mice; Mice, Inbred C57BL; Receptors, Tumor Necrosis Factor, Type I / deficiency; Receptors, Tumor Necrosis Factor, Type I / metabolism; Time Factors; Tumor Necrosis Factor-alpha / metabolism
TL;DR: The results indicate that TAB1- or TAB2-dependent activation of TAK1 is required for maintenance of the hematopoietic system through two mechanisms: one is prevention of TNF-dependent cell death and the other is T NF-independent maintenance of long-term HSC. (via Semantic Scholar)
Sources: Web Of Science, Crossref, NC State University Libraries
Added: August 6, 2018

2011 journal article

Inhibition of autophagy by TAB2 and TAB3

EMBO JOURNAL, 30(24), 4908–4920.

By: A. Criollo*, M. Niso-Santano*, S. Malik*, M. Michaud*, E. Morselli*, G. Marino*, S. Lachkar*, A. Arkhipenko* ...

author keywords: Beclin 1 interactome; mTOR; p53; pifithrin alpha; rapamycin; stress response
TL;DR: The results point to the existence of an autophagy‐stimulatory ‘switch’ whereby TAB2 and TAB3 abandon inhibitory interactions with Beclin 1 to engage in a stimulatory liaison with TAK1. (via Semantic Scholar)
Source: Web Of Science
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.

By: 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
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)
Source: Web Of Science
Added: August 6, 2018

2010 journal article

Ablation of TAK1 Upregulates Reactive Oxygen Species and Selectively Kills Tumor Cells

Cancer Research, 70(21), 8417–8425.

By: E. Omori n, K. Matsumoto n, S. Zhu n, R. Smart n & J. Ninomiya-Tsuji n

MeSH headings : 9,10-Dimethyl-1,2-benzanthracene / toxicity; Animals; Apoptosis; Blotting, Western; Carcinogens / toxicity; Cell Proliferation; Gene Deletion; Integrases / metabolism; Keratinocytes / cytology; Keratinocytes / drug effects; Keratinocytes / metabolism; MAP Kinase Kinase Kinases / antagonists & inhibitors; MAP Kinase Kinase Kinases / physiology; Mice; Mice, Knockout; Papilloma / chemically induced; Papilloma / metabolism; Papilloma / pathology; RNA, Messenger / genetics; RNA, Small Interfering / pharmacology; Reactive Oxygen Species / metabolism; Reverse Transcriptase Polymerase Chain Reaction; Skin / metabolism; Skin / pathology; Skin Neoplasms / chemically induced; Skin Neoplasms / metabolism; Skin Neoplasms / pathology; Up-Regulation
TL;DR: TAK1 kinase could be a new and effective molecular target for ROS-based tumor killing and is examined whether ablation of TAK1 in preexisting skin tumors could cause an increase in ROS and result in tumor cell death. (via Semantic Scholar)
Sources: Web Of Science, Crossref, NC State University Libraries
Added: August 6, 2018

2010 journal article

Regulation of Genotoxic Stress Response by Homeodomain-interacting Protein Kinase 2 through Phosphorylation of Cyclic AMP Response Element-binding Protein at Serine 271

MOLECULAR BIOLOGY OF THE CELL, 21(16), 2966–2974.

By: K. Sakamoto n, B. Huang n, K. Iwasaki n, K. Hailemariam n, J. Ninomiya-Tsuji n & Y. Tsuji n

MeSH headings : Animals; Antineoplastic Agents, Phytogenic / pharmacology; Blotting, Western; Brain-Derived Neurotrophic Factor / genetics; Brain-Derived Neurotrophic Factor / metabolism; CREB-Binding Protein / genetics; CREB-Binding Protein / metabolism; Carrier Proteins / genetics; Carrier Proteins / metabolism; Cell Line, Tumor; Cells, Cultured; Cyclic AMP Response Element-Binding Protein / genetics; Cyclic AMP Response Element-Binding Protein / metabolism; DNA Damage; Embryo, Mammalian / cytology; Etoposide / pharmacology; Fibroblasts / cytology; Fibroblasts / drug effects; Fibroblasts / metabolism; HEK293 Cells; Humans; K562 Cells; Mice; Mice, Knockout; Phosphorylation; Protein Binding; Protein Serine-Threonine Kinases / genetics; Protein Serine-Threonine Kinases / metabolism; RNA Interference; Serine / genetics; Serine / metabolism; Transcription, Genetic / drug effects; Two-Hybrid System Techniques
TL;DR: Homeodomain-interacting protein kinase 2 is a new CREB kinase for phosphorylation at Ser-271 but not Ser-133 in genotoxic stress and activates CREB transactivation function including brain-derived neurotrophic factor (BDNF) mRNA expression. (via Semantic Scholar)
Source: Web Of Science
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, 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
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)
Sources: Web Of Science, Crossref, ORCID, NC State University Libraries
Added: August 6, 2018

2010 journal article

Transforming Growth Factor beta-activated Kinase 1 (TAK1) Kinase Adaptor, TAK1-binding Protein 2, Plays Dual Roles in TAK1 Signaling by Recruiting Both an Activator and an Inhibitor of TAK1 Kinase in Tumor Necrosis Factor Signaling Pathway

JOURNAL OF BIOLOGICAL CHEMISTRY, 285(4), 2333–2339.

By: P. Broglie n, K. Matsumoto*, S. Akira*, D. Brautigan* & J. Ninomiya-Tsuji n

MeSH headings : Adaptor Proteins, Signal Transducing / genetics; Adaptor Proteins, Signal Transducing / metabolism; Animals; Cell Line, Transformed; Dermis / cytology; Fibroblasts / cytology; Fibroblasts / enzymology; Gene Deletion; JNK Mitogen-Activated Protein Kinases / metabolism; MAP Kinase Kinase Kinases / metabolism; MAP Kinase Signaling System / drug effects; MAP Kinase Signaling System / physiology; Mice; NF-kappa B / metabolism; Phosphoprotein Phosphatases / metabolism; Phosphorylation / physiology; Tumor Necrosis Factor-alpha / metabolism; Tumor Necrosis Factor-alpha / pharmacology; Ubiquitin / metabolism; Ubiquitination / physiology
Source: Web Of Science
Added: August 6, 2018

2009 journal article

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

PLOS ONE, 4(2).

By: 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
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)
Source: Web Of Science
Added: August 6, 2018

2009 journal article

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

ONCOGENE, 28(23), 2257–2265.

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)
Source: Web Of Science
Added: August 6, 2018

2008 journal article

203 TAK1 Is Essential for Intestinal Epithelial Cell Survival and Regulates Intestinal Integrity

Gastroenterology, 134(4), A-35-A-36.

By: R. Kajino-Sakamoto, M. Inagaki, J. Kim, S. Robine, K. Matsumoto, C. Jobin, J. Ninomiya-Tsuji*

UN Sustainable Development Goal Categories
2. Zero Hunger (OpenAlex)
Source: Crossref
Added: August 28, 2020

2008 journal article

Enterocyte-derived TAK1 signaling prevents epithelium apoptosis and the development of ileitis and colitis

JOURNAL OF IMMUNOLOGY, 181(2), 1143–1152.

By: R. Kajino-Sakamoto n, M. Inagaki n, E. Lippert*, S. Akira*, S. Robine*, K. Matsumoto*, C. Jobin*, J. Ninomiya-Tsuji n

MeSH headings : Animals; Apoptosis; Colitis / immunology; Colitis / metabolism; Enterocytes / cytology; Enterocytes / immunology; Enterocytes / metabolism; Ileitis / immunology; Ileitis / metabolism; Intestinal Mucosa / immunology; Intestinal Mucosa / metabolism; MAP Kinase Kinase Kinases / immunology; MAP Kinase Kinase Kinases / metabolism; Mice; Mice, Knockout; Mice, Mutant Strains; Signal Transduction; Tumor Necrosis Factor-alpha / immunology; Tumor Necrosis Factor-alpha / metabolism
TL;DR: Enterocyte apoptosis and intestinal inflammation were strongly attenuated when enterocyte-specific constitutive TAK1-deleted mice were crossed to TNF receptor 1−/− mice, and it is proposed that aberration in Tak1 signaling might disrupt intestinal homeostasis and favor the development of inflammatory disease. (via Semantic Scholar)
Source: Web Of Science
Added: August 6, 2018

2008 journal article

Generation of a conditional mutant allele for Tab1 in mouse

GENESIS, 46(8), 431–439.

By: M. Inagaki n, Y. Komatsu*, G. Scott*, G. Yamada*, M. Ray*, J. Ninomiya-Tsuji n, Y. Mishina*

author keywords: conditional gene knockout; MAP kinase; BMP; Tab1; TGF-beta
MeSH headings : Adaptor Proteins, Signal Transducing / genetics; Animals; Exons; Gene Targeting; Integrases / metabolism; Mice; Mutation
TL;DR: It is demonstrated that Cre‐mediated recombination using Sox2‐Cre, a Cre line expressed in the epiblast during early embryogenesis, results in deletion of the gene and protein and homozygous Cre‐recombined null embryos display an identical phenotype to conventional null embryos. (via Semantic Scholar)
UN Sustainable Development Goal Categories
3. Good Health and Well-being (Web of Science; OpenAlex)
Source: Web Of Science
Added: August 6, 2018

2008 journal article

TAB4 stimulates TAK1-TAB1 phosphorylation and binds polyubiquitin to direct signaling to NF-kappa B

JOURNAL OF BIOLOGICAL CHEMISTRY, 283(28), 19245–19254.

By: T. Prickett*, J. Ninomiya-Tsuji n, P. Broglie n, T. Muratore-Schroeder*, J. Shabanowitz*, D. Hunt*, D. Brautigan*

MeSH headings : Adaptor Proteins, Signal Transducing / genetics; Adaptor Proteins, Signal Transducing / metabolism; Amino Acid Motifs / genetics; Amino Acid Substitution; Humans; I-kappa B Kinase / genetics; I-kappa B Kinase / metabolism; Interleukin-1beta / metabolism; MAP Kinase Kinase 3 / genetics; MAP Kinase Kinase 3 / metabolism; MAP Kinase Kinase 6 / genetics; MAP Kinase Kinase 6 / metabolism; MAP Kinase Kinase Kinases / genetics; MAP Kinase Kinase Kinases / metabolism; Mutation, Missense; NF-kappa B / genetics; NF-kappa B / metabolism; Phosphorylation; Protein Binding / genetics; Protein Structure, Tertiary / genetics; Signal Transduction / physiology; Transforming Growth Factor beta / genetics; Transforming Growth Factor beta / metabolism; Ubiquitin / genetics; Ubiquitin / metabolism; p38 Mitogen-Activated Protein Kinases / genetics; p38 Mitogen-Activated Protein Kinases / metabolism
TL;DR: The results show that TAB4 binds TAK1 and polyubiquitin chains to promote specific sites of phosphorylation in TAK 1-TAB1, which activates IKK signaling to NF-κB. (via Semantic Scholar)
Source: Web Of Science
Added: August 6, 2018

2008 journal article

TAK1 is a central mediator of NOD2 signaling in epidermal cells

JOURNAL OF BIOLOGICAL CHEMISTRY, 283(1), 137–144.

By: J. Kim n, E. Omori n, K. Matsumoto*, G. Nunez* & 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)
Source: Web Of Science
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.

By: 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
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)
Source: Web Of Science
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.

By: 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
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)
Source: Web Of Science
Added: August 6, 2018

2007 journal article

Osmotic stress blocks NF-kappa B-dependent in inflammatory responses by inhibiting ubiquitination of I kappa B

FEBS LETTERS, 581(29), 5549–5554.

By: W. HuangFu n, K. Matsumoto* & J. Ninomiya-Tsuji n

author keywords: NF-kappa B; cytokine; osmotic stress; inflammation
MeSH headings : Animals; Cells, Cultured; Humans; I-kappa B Kinase / metabolism; I-kappa B Proteins / antagonists & inhibitors; I-kappa B Proteins / metabolism; Inflammation / metabolism; Interleukin-1 / antagonists & inhibitors; Interleukin-1 / metabolism; Mice; Mice, Inbred C57BL; NF-KappaB Inhibitor alpha; NF-kappa B / antagonists & inhibitors; NF-kappa B / metabolism; Osmotic Pressure; Signal Transduction; Ubiquitination / physiology
TL;DR: Osmotic stress‐mediated modification of the NF‐κB pathway, a central signaling pathway in inflammation, is investigated and blockage of IκBα ubiquitination is likely to be a major mechanism for inhibition of inflammation by hypertonic conditions. (via Semantic Scholar)
Source: Web Of Science
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.

By: 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
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)
Source: Web Of Science
Added: August 6, 2018

2006 journal article

Osmotic Stress Activates the TAK1-JNK Pathway While Blocking TAK1-mediated NF-κB Activation

Journal of Biological Chemistry, 281(39), 28802–28810.

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

MeSH headings : Animals; Cell Line; Enzyme Activation; Gene Expression Regulation, Enzymologic; Humans; MAP Kinase Kinase 4 / metabolism; MAP Kinase Kinase Kinases / metabolism; Mice; NF-kappa B / metabolism; Osmosis; Protein Binding; Protein Kinases / chemistry; Protein Kinases / physiology; Protein Serine-Threonine Kinases / physiology; RNA, Small Interfering / metabolism
TL;DR: It is found that TAK1 is essential for osmotic stress-induced activation of JNK but is not an exclusive mediator of p38 activation, and TAO2 (thousand-and-one amino acid kinase 2) associates with Tak1 and can inhibit TAK 1-mediated activation of NF-κB but not of J NK. (via Semantic Scholar)
Source: Crossref
Added: August 28, 2020

2006 journal article

Osmotic stress activates the TAK1-JNK pathway while blocking TAK1-mediated NF-kappa B activation - TAO2 regulates TAK1 pathways

Journal of Biological Chemistry, 281(39), 28802–28810.

By: W. Huangfu, E. Omori, S. Akira, K. Matsumoto & J. Ninomiya-Tsuji

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

2006 journal article

Protein phosphatase 6 down-regulates TAK1 kinase activation in the IL-1 signaling pathway

JOURNAL OF BIOLOGICAL CHEMISTRY, 281(52), 39891–39896.

By: T. Kajino*, H. Ren*, S. Iemura*, T. Natsume*, B. Stefansson*, D. Brautigan*, K. Matsumoto*, J. Ninomiya-Tsuji n

MeSH headings : Cells, Cultured; Down-Regulation / drug effects; Down-Regulation / physiology; Enzyme Activation / physiology; Enzyme Inhibitors / pharmacology; Humans; Interleukin-1 / physiology; Isoenzymes / antagonists & inhibitors; Isoenzymes / biosynthesis; Isoenzymes / physiology; MAP Kinase Kinase Kinases / antagonists & inhibitors; MAP Kinase Kinase Kinases / metabolism; MAP Kinase Kinase Kinases / physiology; Phosphoprotein Phosphatases / antagonists & inhibitors; Phosphoprotein Phosphatases / biosynthesis; Phosphoprotein Phosphatases / physiology; Phosphorylation / drug effects; Signal Transduction / drug effects; Signal Transduction / physiology; Up-Regulation / drug effects
TL;DR: It is found that toxin inhibition of type 2A protein phosphatases greatly enhances interleukin 1 (IL-1)-dependent phosphorylation of Thr-187 in the TAK1 activation loop as well as the catalytic activity of Tak1. (via Semantic Scholar)
Source: Web Of Science
Added: August 6, 2018

2006 journal article

TAK1 is a component of the Epstein-Barr virus LMP1 complex and is essential for activation of JNK but not of NF-kappa B

JOURNAL OF BIOLOGICAL CHEMISTRY, 281(12), 7863–7872.

By: N. Uemura n, T. Kajino*, H. Sanjo*, S. Sato*, S. Akira*, K. Matsumoto*, J. Ninomiya-Tsuji n

MeSH headings : Animals; Cell Line; Cytoplasm / metabolism; Enzyme Activation; Enzyme Inhibitors / pharmacology; Fibroblasts / metabolism; Gene Deletion; Herpesvirus 4, Human / metabolism; Humans; Immunoblotting; MAP Kinase Kinase 4 / metabolism; MAP Kinase Kinase Kinases / metabolism; MAP Kinase Kinase Kinases / physiology; Mice; Mice, Transgenic; Models, Biological; Mutation; NF-kappa B / metabolism; Plasmids / metabolism; Signal Transduction; TNF Receptor-Associated Factor 6 / metabolism; Transfection; Viral Matrix Proteins / metabolism
TL;DR: Results suggest that an LMP1-associated complex containing TRAF6, TAB2, and TAK1 plays an essential role in the activation of JNK, however, TAK 1 is not an exclusive intermediate for NF-κB activation in L MP1 signaling. (via Semantic Scholar)
Source: Web Of Science
Added: August 6, 2018

2006 journal article

TAK1 is a master regulator of epidermal homeostasis involving skin inflammation and apoptosis

JOURNAL OF BIOLOGICAL CHEMISTRY, 281(28), 19610–19617.

By: E. Omori n, K. Matsumoto*, H. Sanjo*, S. Sato*, S. Akira*, R. Smart n, J. Ninomiya-Tsuji n

MeSH headings : Animals; Apoptosis; Cytokines / metabolism; Epidermis / metabolism; Gene Deletion; Homeostasis; Inflammation; Keratinocytes / cytology; Keratinocytes / metabolism; MAP Kinase Kinase 4 / metabolism; MAP Kinase Kinase Kinases / physiology; Mice; Mice, Inbred C57BL; NF-kappa B / metabolism; Skin / pathology
TL;DR: It is demonstrated that TAK1 is the major regulator of skin inflammation as well as keratinocyte death in vivo and is a master regulator of TNF signaling in skin and regulates skin inflammation and keratinocytes death. (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
Added: August 6, 2018

2006 journal article

TAK1 is indispensable for development of T cells and prevention of colitis by the generation of regulatory T cells

INTERNATIONAL IMMUNOLOGY, 18(10), 1405–1411.

By: S. Sato*, H. Sanjo, T. Tsujimura, J. Ninomiya-Tsuji, M. Yamamoto, T. Kawai, O. Takeuchi, S. Akira

author keywords: IBD; regulatory T cells; signal transduction; TCR
MeSH headings : Aging / genetics; Aging / immunology; Aging / pathology; Animals; B-Lymphocytes / immunology; B-Lymphocytes / pathology; CD8-Positive T-Lymphocytes / immunology; CD8-Positive T-Lymphocytes / pathology; Colitis / genetics; Colitis / immunology; Colitis / pathology; Colitis / prevention & control; Humans; MAP Kinase Kinase Kinases / deficiency; MAP Kinase Kinase Kinases / immunology; MAP Kinase Signaling System / genetics; MAP Kinase Signaling System / immunology; Mice; Mice, Knockout; T-Lymphocytes, Regulatory / immunology; T-Lymphocytes, Regulatory / pathology; Thymus Gland / immunology; Thymus Gland / pathology
TL;DR: The results show that TAK1, by controlling the generation of central Treg cells, is important for preventing spontaneously developing colitis. (via Semantic Scholar)
Source: Web Of Science
Added: August 6, 2018

2006 journal article

Tab1

AfCS-Nature Molecule Pages.

By: J. Ninomiya-Tsuji* & K. Matsumoto

Source: Crossref
Added: August 28, 2020

2006 journal article

Tak1

AfCS-Nature Molecule Pages.

By: J. Ninomiya-Tsuji* & K. Matsumoto

Source: Crossref
Added: August 28, 2020

2005 journal article

AMP-activated protein kinase activates p38 mitogen-activated protein kinase by increasing recruitment of p38 MAPK to TAB1 in the ischemic heart

CIRCULATION RESEARCH, 97(9), 872–879.

By: J. Li n, E. Miller n, J. Ninomiya-Tsuji n, R. Russell n & L. Young n

author keywords: ischemia; AMP-activated protein kinase; p38 MAPK mitogen-activated protein kinase; transforming growth factor-beta-activated protein kinase 1-binding protein 1; glucose transport
MeSH headings : AMP-Activated Protein Kinases; Aminoimidazole Carboxamide / analogs & derivatives; Aminoimidazole Carboxamide / pharmacology; Animals; Anisomycin / pharmacology; Cell Hypoxia; Enzyme Activation; Glucose / metabolism; Glucose Transporter Type 4 / metabolism; Intracellular Signaling Peptides and Proteins / metabolism; MAP Kinase Kinase 3 / physiology; Male; Mice; Mice, Inbred C57BL; Mice, Transgenic; Multienzyme Complexes / physiology; Myocardial Ischemia / enzymology; Protein Serine-Threonine Kinases / physiology; Protein Transport; Rats; Rats, Sprague-Dawley; Ribonucleotides / pharmacology; p38 Mitogen-Activated Protein Kinases / metabolism
TL;DR: AMP-activated protein kinase has an important role in promoting p38 MAPK activation in the ischemic heart by inducing p38MAPK autophosphorylation through interaction with the scaffold protein TAB1. (via Semantic Scholar)
Source: Web Of Science
Added: August 6, 2018

2005 journal article

Essential function for the kinase TAK1 in innate and adaptive immune responses

NATURE IMMUNOLOGY, 6(11), 1087–1095.

MeSH headings : Animals; B-Lymphocytes / drug effects; B-Lymphocytes / enzymology; B-Lymphocytes / immunology; CD40 Antigens / pharmacology; Embryo, Mammalian / cytology; Fibroblasts / drug effects; Fibroblasts / enzymology; Gene Deletion; Immunity, Innate; Interleukin-17 / pharmacology; Lymphopoiesis; MAP Kinase Kinase Kinases / deficiency; MAP Kinase Kinase Kinases / genetics; MAP Kinase Kinase Kinases / physiology; Membrane Glycoproteins / immunology; Mice; Mice, Mutant Strains; NF-kappa B / pharmacology; Receptors, Antigen, B-Cell / agonists; Receptors, Antigen, B-Cell / immunology; Receptors, Cell Surface / immunology; Toll-Like Receptors; Tumor Necrosis Factor-alpha / pharmacology
TL;DR: It is shown that TAK1 is key in the cellular response to a variety of stimuli and was indispensable for cellular responses to Toll-like receptor ligands, CD40 and B cell receptor crosslinking. (via Semantic Scholar)
UN Sustainable Development Goal Categories
Source: Web Of Science
Added: August 6, 2018

2005 journal article

TAK1-binding protein 2 facilitates ubiquitination of TRAF6 and assembly of TRAF6 with IKK in the IL-1 signaling pathway

GENES TO CELLS, 10(5), 447–454.

By: S. Kishida n, H. Sanjo*, S. Akira*, K. Matsumoto* & J. Ninomiya-Tsuji n

MeSH headings : Adaptor Proteins, Signal Transducing / genetics; Adaptor Proteins, Signal Transducing / metabolism; Animals; I-kappa B Kinase; Interleukin-1 / metabolism; Mice; Mutation; NF-kappa B / metabolism; Protein Serine-Threonine Kinases / metabolism; Protein Structure, Tertiary; Signal Transduction / physiology; TNF Receptor-Associated Factor 6 / metabolism; Ubiquitin / metabolism
TL;DR: TAK1‐binding protein 2 (TAB2) functions to facilitate TRAF6 ubiquitination and thereby mediates IL‐1‐induced cellular events, and a conserved ubiquitin binding domain in TAB2, the CUE domain, is important for this function. (via Semantic Scholar)
Source: Web Of Science
Added: August 6, 2018

2005 journal article

Transforming growth factor beta-activated kinase 1 is a key mediator of ovine follicle-stimulating hormone beta-subunit expression

ENDOCRINOLOGY, 146(11), 4814–4824.

By: N. Safwat n, J. Ninomiya-Tsuji n, A. Gore n & W. Miller n

MeSH headings : Activins / pharmacology; Animals; Cell Line; Enzyme Activation / physiology; Follicle Stimulating Hormone, beta Subunit / antagonists & inhibitors; Follicle Stimulating Hormone, beta Subunit / biosynthesis; Follicle Stimulating Hormone, beta Subunit / genetics; Follicle Stimulating Hormone, beta Subunit / metabolism; Humans; Inhibin-beta Subunits / pharmacology; Kinetics; Lactones / pharmacology; Luciferases / genetics; MAP Kinase Kinase Kinases / metabolism; Phosphorylation; Recombinant Fusion Proteins / biosynthesis; Recombinant Proteins / pharmacology; Resorcinols / pharmacology; Sheep; Transfection; p38 Mitogen-Activated Protein Kinases / metabolism
TL;DR: This study used 4.7 kb of the ovine FSHβ-promoter linked to luciferase (oFSHβLuc) plus a well-characterized activin-responsive construct, p3TPLuc, to investigate the hypothesis that Smad3, TGFβ-activated kinase 1 (TAK1), or both cause activationin-mediated induction of FSH. (via Semantic Scholar)
Source: Web Of Science
Added: August 6, 2018

2004 journal article

Activation mechanism of c-Jun amino-terminal kinase in the course of neural differentiation of P19 embryonic carcinoma cells

JOURNAL OF BIOLOGICAL CHEMISTRY, 279(35), 36616–36620.

By: S. Akiyama*, T. Yonezawa*, T. Kudo*, M. Li*, H. Wang*, M. Ito*, K. Yoshioka*, J. Ninomiya-Tsuji n ...

MeSH headings : Animals; Blotting, Northern; Carcinoma, Embryonal / metabolism; Cell Differentiation; Cell Line; Cell Line, Tumor; Cell Nucleus / metabolism; Enzyme Activation; Fluorescent Antibody Technique, Indirect; Gene Expression Regulation, Developmental; JNK Mitogen-Activated Protein Kinases; MAP Kinase Kinase Kinase 4; MAP Kinase Kinase Kinases / metabolism; Mice; Microscopy, Confocal; Mitogen-Activated Protein Kinases / metabolism; Neurons / metabolism; Phosphoprotein Phosphatases / metabolism; Precipitin Tests; Protein Phosphatase 2C; Signal Transduction; Transfection; Tretinoin / metabolism; Tubulin / metabolism
TL;DR: It is demonstrated that activities of MAPK kinase 4 and TAK1, one of the upstream kinases of MKK4, were enhanced in the neurally differentiating cells and suggest that two distinct TAK 1-MKK4-JNK signaling pathways are independently activated at the different intracellular locations and may participate in the regulation of the neural differentiation of P19 cells. (via Semantic Scholar)
Source: Web Of Science
Added: August 6, 2018

2004 journal article

Involvement of ASK1 in Ca 2+ ‐induced p38 MAP kinase activation

EMBO Reports, 5(2), 161–166.

MeSH headings : Animals; Calcium / metabolism; Calcium / pharmacology; Calcium Signaling; Calcium-Calmodulin-Dependent Protein Kinase Type 2; Calcium-Calmodulin-Dependent Protein Kinases / metabolism; Cells, Cultured; Fibroblasts / drug effects; Fibroblasts / metabolism; Glutathione Transferase / analysis; MAP Kinase Kinase Kinase 5 / metabolism; MAP Kinase Kinase Kinase 5 / physiology; MAP Kinase Signaling System / physiology; Marine Toxins / pharmacology; Mice; Mice, Inbred C57BL; Oxocins / pharmacology; Phosphorylation; Potassium Channels, Calcium-Activated / metabolism; RNA, Small Interfering / pharmacology; Synaptosomes / drug effects; Synaptosomes / metabolism; p38 Mitogen-Activated Protein Kinases / metabolism
TL;DR: It is shown that Ca2+ signalling regulates the ASK1–p38 MAP kinase cascade, which is a critical intermediate of Ca2- signalling between CaMKII and p38 MAP Kinase. (via Semantic Scholar)
Source: Crossref
Added: January 5, 2021

2003 journal article

A dominant negative TAK1 inhibits cellular fibrotic responses induced by TGF-beta

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 307(2), 332–337.

By: K. Ono, T. Ohtomo, J. Ninomiya-Tsuji n & M. Tsuchiya

author keywords: transforming growth factor-beta; TGF-beta activated kinase 1; dominant negative inhibitor; fibrotic marker proteins
MeSH headings : Adaptor Proteins, Signal Transducing; Animals; Biomarkers; Carrier Proteins / metabolism; Cell Line; Collagen Type I / metabolism; Collagen Type IV / metabolism; Extracellular Matrix / metabolism; Fibronectins / metabolism; Fibrosis / metabolism; Humans; Intracellular Signaling Peptides and Proteins; MAP Kinase Kinase Kinases / genetics; MAP Kinase Kinase Kinases / metabolism; Plasminogen Activator Inhibitor 1 / metabolism; Protein Binding; Signal Transduction / physiology; Transforming Growth Factor beta / metabolism; Two-Hybrid System Techniques
TL;DR: A minimal portion of TAK1 lacking kinase activity that binds to TAB1 was designed as a Tak1 dominant negative inhibitor (TAK1-DN) that decreased the ECM protein production, indicating that TAK 1-DN retains the ability to intercept the TGF-beta signaling effectively. (via Semantic Scholar)
UN Sustainable Development Goal Categories
Source: Web Of Science
Added: August 6, 2018

2003 journal article

A resorcylic acid lactone, 5Z-7-oxozeaenol, prevents inflammation by inhibiting the catalytic activity of TAK1 MAPK kinase kinase

JOURNAL OF BIOLOGICAL CHEMISTRY, 278(20), 18485–18490.

By: J. Ninomiya-Tsuji n, T. Kajino*, K. Ono, T. Ohtomo, M. Matsumoto, M. Shiina, M. Mihara, M. Tsuchiya, K. Matsumoto*

MeSH headings : Animals; Anti-Inflammatory Agents / chemistry; Anti-Inflammatory Agents / pharmacology; Cell Line; Cells, Cultured; Cyclooxygenase 2; Dose-Response Relationship, Drug; Enzyme Activation; Female; Genes, Reporter; Genetic Vectors; Humans; Immunoblotting; Inflammation; Inhibitory Concentration 50; Interleukin-1 / metabolism; Isoenzymes / metabolism; Lactones / chemistry; MAP Kinase Kinase Kinases / metabolism; MAP Kinase Signaling System; Membrane Proteins; Mice; Mice, Inbred BALB C; Mitogen-Activated Protein Kinases / metabolism; Models, Chemical; Precipitin Tests; Prostaglandin-Endoperoxide Synthases / metabolism; Protein Binding; Signal Transduction; Time Factors; Transfection; Zearalenone / analogs & derivatives; Zearalenone / chemistry; Zearalenone / pharmacology; p38 Mitogen-Activated Protein Kinases
TL;DR: 5Z-7-oxozeaenol blocks proinflammatory signaling by selectively inhibiting TAK1 MAPKKK, resulting in inhibition of cyclooxgenase-2 production in cell culture and in vivo. (via Semantic Scholar)
Source: Web Of Science
Added: August 6, 2018

2003 journal article

Regulation of the interleukin-1-induced signaling pathways by a novel member of the protein phosphatase 2C family (PP2C epsilon)

JOURNAL OF BIOLOGICAL CHEMISTRY, 278(14), 12013–12021.

By: M. Li*, K. Katsura*, H. Nomiyama*, K. Komaki*, J. Ninomiya-Tsuji n, K. Matsumoto*, T. Kobayashi*, S. Tamura*

MeSH headings : Amino Acid Sequence; Animals; Base Sequence; Calcium-Calmodulin-Dependent Protein Kinases / metabolism; Escherichia coli; Gene Expression Regulation, Enzymologic; Genes, Reporter; In Vitro Techniques; Interleukin-1 / pharmacology; JNK Mitogen-Activated Protein Kinases; MAP Kinase Kinase 3; MAP Kinase Kinase 4; MAP Kinase Kinase 6; MAP Kinase Kinase Kinases / metabolism; Mice; Mitogen-Activated Protein Kinase Kinases / metabolism; Mitogen-Activated Protein Kinases / metabolism; Molecular Sequence Data; Phosphoprotein Phosphatases / genetics; Phosphoprotein Phosphatases / metabolism; Phosphorylation; Point Mutation; Protein Phosphatase 2C; Protein-Tyrosine Kinases / metabolism; Signal Transduction / drug effects; Signal Transduction / physiology; Transcription Factor AP-1 / genetics; p38 Mitogen-Activated Protein Kinases
TL;DR: Results suggest that, in the absence of IL-1-induced signal, PP2Cε contributes to keeping the TAK1 signaling pathway in an inactive state by associating with and dephosphorylating TAK 1. (via Semantic Scholar)
Source: Web Of Science
Added: August 6, 2018

2003 journal article

TAK1 is critical for I kappa B kinase-mediated activation of the NF-kappa B pathway

JOURNAL OF MOLECULAR BIOLOGY, 326(1), 105–115.

By: G. Takaesu*, R. Surabhi*, K. Park*, J. Ninomiya-Tsuji n, K. Matsumoto* & R. Gaynor*

author keywords: NF-kappa B; I kappa B kinase; TAK1; signal transduction; RNA interference
MeSH headings : Enzyme Activation / drug effects; Gene Expression; HeLa Cells; Humans; I-kappa B Kinase; Interleukin-1 / pharmacology; MAP Kinase Kinase Kinases / genetics; MAP Kinase Kinase Kinases / metabolism; NF-kappa B / metabolism; Protein Serine-Threonine Kinases / genetics; Protein Serine-Threonine Kinases / metabolism; Proteins / genetics; Proteins / metabolism; RNA, Messenger / genetics; RNA, Messenger / metabolism; RNA, Small Interfering / genetics; RNA, Small Interfering / metabolism; Signal Transduction / drug effects; TNF Receptor-Associated Factor 2; Transfection; Tumor Necrosis Factor-alpha / pharmacology
TL;DR: Small interfering RNAs directed against IKKα, IKKβ and the upstream regulatory kinase TAK1 were utilized in order to better define their roles in cytokine-induced activation of the NF-κB pathway. (via Semantic Scholar)
UN Sustainable Development Goal Categories
Source: Web Of Science
Added: August 6, 2018

2002 journal article

Targeted disruption of the Tab1 gene causes embryonic lethality and defects in cardiovascular and lung morphogenesis

MECHANISMS OF DEVELOPMENT, 119(2), 239–249.

author keywords: bone morphogenetic protein; mitogen-activated protein kinase; mouse; signal transduction; TGF-beta activated kinase-1 binding protein-1; TGF-beta activated kinase-1; transforming growth factor-beta
MeSH headings : Adaptor Proteins, Signal Transducing; Alleles; Amino Acid Sequence; Animals; Blotting, Western; Cell Differentiation; Cell Division; Cloning, Molecular; Genotype; HIV Envelope Protein gp120 / genetics; HIV Envelope Protein gp120 / physiology; Heart / embryology; Homozygote; Humans; Immunoblotting; In Situ Hybridization; Luciferases / metabolism; Lung / embryology; MAP Kinase Kinase Kinases / metabolism; Mice; Models, Genetic; Molecular Sequence Data; Mutagenesis, Site-Directed; Mutation; Oligonucleotides, Antisense / pharmacology; Recombinant Fusion Proteins / genetics; Recombinant Fusion Proteins / physiology; Recombination, Genetic; Reverse Transcriptase Polymerase Chain Reaction; Signal Transduction; Time Factors; Tissue Distribution; Transfection; Transforming Growth Factor beta / metabolism
TL;DR: A possibility that TAB1 plays an important role in mammalian embryogenesis and is required for TAK1 activation in TGF-beta signaling is indicated. (via Semantic Scholar)
UN Sustainable Development Goal Categories
3. Good Health and Well-being (Web of Science; OpenAlex)
Source: Web Of Science
Added: August 6, 2018

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