Kazuhito Sai

Works (6)

Updated: December 3rd, 2024 05:02

2024 article

TAK1 inhibition translocates pore-forming proteins, MLKL and gasdermins into mitochondria to generate reactive oxygen species

Gonzalez-Calderon, R., Lopez-Perez, W., Sai, K., & Ninomiya-Tsuji, J. (2024, March). JOURNAL OF BIOLOGICAL CHEMISTRY, Vol. 300, pp. S555–S555.

By: R. Gonzalez-Calderon n, W. Lopez-Perez  n, K. Sai n & J. Ninomiya-Tsuji n 

Sources: Web Of Science, NC State University Libraries
Added: December 2, 2024

2024 article

The Mechanism and Roles of TAK1 hyperactivation in the Alzheimer's Disease Mouse Model

Nakanishi-Hester, A., Sai, K., & Ninomiya-Tsuji, J. (2024, March). JOURNAL OF BIOLOGICAL CHEMISTRY, Vol. 300, pp. S556–S556.

By: A. Nakanishi-Hester n , K. Sai n & J. Ninomiya-Tsuji n 

Sources: Web Of Science, NC State University Libraries
Added: December 2, 2024

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)
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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 

Contributors: W. López-Pérez  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)
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Sources: Web Of Science, NC State University Libraries, ORCID
Added: July 12, 2021

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)
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Sources: Web Of Science, ORCID, NC State University Libraries
Added: June 24, 2019

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 

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
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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Sources: Web Of Science, NC State University Libraries, ORCID
Added: August 6, 2018

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