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Signal-transducing adaptor protein-2 has a nonredundant role for IL-33-triggered mast cell activation

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/87011

Title: Signal-transducing adaptor protein-2 has a nonredundant role for IL-33-triggered mast cell activation
Authors: Kashiwakura, Jun-ichi Browse this author →KAKEN DB
Koizumi, Nao Browse this author
Saitoh, Kodai Browse this author
Kagohashi, Kota Browse this author
Sasaki, Yuto Browse this author
Kobayashi, Fuki Browse this author
Kawahara, Shoya Browse this author
Yamauchi, Yukie Browse this author
Kitai, Yuichi Browse this author →KAKEN DB
Muromoto, Ryuta Browse this author →KAKEN DB
Oritani, Kenji Browse this author →KAKEN DB
Matsuda, Tadashi Browse this author →KAKEN DB
Keywords: Mast cells
IL-33
Signal-transducing adaptor molecule-2
ST2
NF-kappa B
Issue Date: 1-Oct-2021
Publisher: Elsevier
Journal Title: Biochemical and biophysical research communications
Volume: 572
Start Page: 80
End Page: 85
Publisher DOI: 10.1016/j.bbrc.2021.07.098
Abstract: Signal-transducing adaptor protein (STAP)-2 is one of the STAP family adaptor proteins and ubiquitously expressed in a variety types of cells. Although STAP-2 is required for modification of Fc epsilon RI signal transduction in mast cells, other involvement of STAP-2 in mast cell functions is unknown, yet. In the present study, we mainly investigated functional roles of STAP-2 in IL-33-induced mast cell activation. In STAP-2-deficient, but not STAP-1-deficient, mast cells, IL-33-induced IL-6 and TNF-alpha production was significantly decreased compared with that of wild-type mast cells. In addition, STAP-2-deficiency greatly reduced TLR4-mediated mast cell activation and cytokine production. For the mechanisms, STAP-2 directly binds to IKK alpha after IL-33 stimulation, leading to elevated NF-kappa B activity. In conclusion, STAP-2, but not STAP-1, participates in IL-33-induced mast cells activation.
Rights: © 2021. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/
http://creativecommons.org/licenses/by-nc-nd/4.0/
Type: article (author version)
URI: http://hdl.handle.net/2115/87011
Appears in Collections:薬学研究院 (Faculty of Pharmaceutical Sciences) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 柏倉 淳一

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