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• TAK1-binding proteins (TAB)2 and TAB3 are redundantly required for TLR-induced cytokine production in macrophages

  Tanveer Ali, Huong Minh Nguyen, Naeem Abbas, Osamu Takeuchi, Shizuo Akira, Toshihiko Suzuki, Goro Matsuzaki, Giichi Takaesu

  International Immunology ( Oxford University Press )    2024.04 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

  　View Summary

  Transforming growth factor-β-activated kinase 1 (TAK1) plays a pivotal role in innate and adaptive immunity. TAK1 is essential for the activation of mitogen-activated protein kinases (MAPKs) and nuclear factor (NF)-κB pathways downstream of diverse immune receptors, including Toll-like receptors (TLRs). Upon stimulation with TLR ligands, TAK1 is activated via recruitment to lysine 63-linked polyubiquitin chain through TAK1-binding proteins (TAB) 2 and TAB3. However, the physiological importance of TAB2 and TAB3 in macrophages is still controversial. A previous study has shown that mouse bone marrow-derived macrophages (BMDMs) isolated from mice double deficient for TAB2 and TAB3 produced tumor necrosis factor (TNF)-α and interleukin (IL)-6 to the similar levels as control wild-type BMDMs in response to TLR ligands such as lipopolysaccharide (LPS) or Pam3CSK4, indicating that TAB2 and TAB3 are dispensable for TLR signaling. In this study, we revisited the role of TAB2 and TAB3 using an improved mouse model. We observed a significant impairment in the production of pro-inflammatory cytokines and chemokine in LPS- or Pam3CSK4-treated BMDMs deficient for both TAB2 and TAB3. Double deficiency of TAB2 and TAB3 resulted in the decreased activation of NF-κB and MAPK pathways as well as the slight decrease in TAK1 activation in response to LPS or Pam3CSK4. Notably, the TLR-mediated expression of inhibitor of NF-κB (IκB)ζ was severely compromised at the protein and mRNA levels in the TAB2/TAB3 double-deficient BMDMs, thereby impeding IL-6 production. Our results suggest that TAB2 and TAB3 play a redundant and indispensable role in TLR signaling pathway.

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• GRIM-19 is a target of mycobacterial Zn²⁺ metalloprotease 1 and indispensable for NLRP3 inflammasome activation

  Kurane T.

  FASEB Journal ( FASEB Journal )  36 ( 1 ) e22096   2022.01 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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  Tuberculosis is a communicable disease caused by Mycobacterium tuberculosis which primarily infects macrophages and establishes intracellular parasitism. A mycobacterial virulence factor Zn2+ metalloprotease 1 (Zmp1) is known to suppress interleukin (IL)-1β production by inhibiting caspase-1 resulting in phagosome maturation arrest. However, the molecular mechanism of caspase-1 inhibition by Zmp1 is still elusive. Here, we identified GRIM-19 (also known as NDUFA13), an essential subunit of mitochondrial respiratory chain complex I, as a novel Zmp1-binding protein. Using the CRISPR/Cas9 system, we generated GRIM-19 knockout murine macrophage cell line J774.1 and found that GRIM-19 is essential for IL-1β production during mycobacterial infection as well as in response to NLRP3 inflammasome-activating stimuli such as extracellular ATP or nigericin. We also found that GRIM-19 is required for the generation of mitochondrial reactive oxygen species and NLRP3-dependent activation of caspase-1. Loss of GRIM-19 or forced expression of Zmp1 resulted in a decrease in mitochondrial membrane potential. Our study revealed a previously unrecognized role of GRIM-19 as an essential regulator of NLRP3 inflammasome and a molecular mechanism underlying Zmp1-mediated suppression of IL-1β production during mycobacterial infection.

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• miR-935 Inhibits Oral Squamous Cell Carcinoma and Targets Inositol Polyphosphate-4-phosphatase Type IA (INPP4A).

  Maruyama N, Umikawa M, Matsumoto H, Maruyama T, Nishihara K, Nakasone T, Matayoshi A, Goto T, Hirano F, Arasaki A, Nakamura H, Matsuzaki G, Takaesu G

  Anticancer research ( Anticancer Research )  40 ( 11 ) 6101 - 6113   2020.11 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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  BACKGROUND/AIM: Oral squamous cell carcinoma (OSCC) is a common malignancy with poor prognosis. Therefore, novel therapeutic options are needed to improve prognosis of OSCC. Recently, microRNAs (miRs) have received increasing attention as a potential therapeutic tool for carcinomas. However, no definitive miR-based drugs for patients with OSCC have been reported to date. The aim of this study was to identify new miRs potentially involved in cellular processes associated with OSCC malignancy, which could lead to novel therapeutic strategies. MATERIALS AND METHODS: We identified miRs that are modulated in OSCC and possibly regulate OSCC malignancy, using miR microarray on OSCC cell lines. RESULTS: miR-935 and miR-509-3p were down-regulated in OSCC cell lines and patient tissues. When miR-935 was overexpressed in HSC-3-M3 cells, proliferation, migration, and invasion of the cell line was suppressed, whereas apoptosis was increased. Moreover, we showed that the gene inositol polyphosphate-4-phosphatase type I A (INPP4A) is a potential target whose expression is positively regulated by miR-935. CONCLUSION: miR-935 may function as a tumor suppressor by inhibiting OSCC malignancy via INPP4A induction. Therefore, miR-935 can be a new therapeutic candidate for OSCC treatment.

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• Effects of Psidium guajava leaf extract on secretion systems of Gram-negative enteropathogenic bacteria.

  Nakasone N, Ogura Y, Higa N, Toma C, Koizumi Y, Takaesu G, Suzuki T, Yamashiro T

  Microbiology and immunology ( Microbiology and Immunology )  62 ( 7 ) 444 - 453   2018.05 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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• Involvement of IL-17A-producing TCR y delta T cells in late protective immunity against pulmonary Mycobacterium tuberculosis infection

  Umemura Masayuki, Okamoto-Yoshida Yuko, Yahagi Ayano, Nakae Susumu, Iwakura Yoichiro, Takaesu Giichi, Matsuzaki Goro

  JOURNAL OF IMMUNOLOGY   198 ( 1 )   2017.05 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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• マイコバクテリア感染肺に誘導されるIL‐17A産生細胞の多様性

  梅村正幸, 儀間香南子, 高江洲義一, 中江進, 岩倉洋一郎, 松崎吾朗

  日本インターフェロン・サイトカイン学会学術集会抄録集   83   96   2018.07

   

• Two types of TRAF6-dependent TAK1 activation in the IL-1 signaling pathway

  Giichi Takaesu

  Biotarget   2 ( 1 )   2018.01

   

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Presentations 【 display / non-display 】

• A molecular mechanism of IL-1β inhibition by mycobacterial effector protein

  Tomomi Kurane, Kazuko Sawada, Giichi Takaesu, Masayuki Umemura, Goro Matsuzaki

  The 93rd Annual Meeting of Japanese Society for Bacteriology  2020.02  -  2020.02 

• Identification and functional analysis of a host protein targeted by mycobacterial effector Zmp1

  Giichi Takaesu, Masayuki Umemura, Goro Matsuzaki

  The 93rd Annual Meeting of Japanese Society for Bacteriology  2020.02  -  2020.02 

• Mechanism of mycobacteria specific IL-17A production of BCG infected lung-derived TCRgammadelta T cells

  梅村 正幸, 飯村 澪, 藏根 友美, 高江洲 義一, 松崎 吾朗

  第48回日本免疫学会学術集会  2019.12  -  2019.12 

• Molecular basis of a mycobacterial effector protein for the development of host-directed therapy of tuberculosis

  Giichi Takaesu, Tomomi Kurane, Kazuko Sawada, Masayuki Umemura, Goro Matsuzaki

  The 42nd Annual Meeting of the Molecular Biology Society of Japan  2019.12  -  2019.12 

• A molecular mechanism of IL-1β suppression by mycobacterial effector protein

  Giichi Takaesu, Tomomi Kurane, Kazuko Sawada, Masayuki Umemura, Goro Matsuzaki

  The 60th Annual Meeting for the Japanese Society of Tropical Medicine  2019.11  -  2019.11 

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• Grant-in-Aid for Scientific Research(B)

  Project Year: 2020.04  -  2023.03 

  Direct: 13,500,000 (YEN)  Overheads: 17,550,000 (YEN)  Total: 4,050,000 (YEN)

• Grant-in-Aid for Scientific Research(B)

  Project Year: 2020.04  -  2023.03 

  Direct: 13,500,000 (YEN)  Overheads: 17,550,000 (YEN)  Total: 4,050,000 (YEN)

• Grant-in-Aid for Scientific Research(C)

  Project Year: 2018.04  -  2021.03 

  Direct: 3,400,000 (YEN)  Overheads: 1,020,000 (YEN)  Total: 4,420,000 (YEN)

• Grant-in-Aid for Scientific Research(C)

  Project Year: 2018.04  -  2021.03 

  Direct: 3,400,000 (YEN)  Overheads: 4,420,000 (YEN)  Total: 1,020,000 (YEN)

• Grant-in-Aid for Scientific Research(C)

  Project Year: 2018.04  -  2021.03 

  Direct: 3,400,000 (YEN)  Overheads: 4,420,000 (YEN)  Total: 1,020,000 (YEN)

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• 2024.02

  　

  　

  

• 2023.12

  　

  　

  

• 2023.11

  　

  　

  

• 2023.11

  　

  　

  

• 2023.10

  　

  　

  

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