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STAP-2 interacts with Pyk2 and enhances Pyk2 activity in T-cells

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Title: STAP-2 interacts with Pyk2 and enhances Pyk2 activity in T-cells
Authors: Saitoh, Kodai Browse this author
Tsuchiya, Takuya Browse this author
Kashiwakura, Jun-ichi Browse this author
Muromoto, Ryuta Browse this author →KAKEN DB
Kitai, Yuichi Browse this author →KAKEN DB
Sekine, Yuichi Browse this author
Oritani, Kenji Browse this author
Matsuda, Tadashi Browse this author →KAKEN DB
Keywords: Pyk2
SDF-l alpha
Issue Date: 17-Jun-2017
Publisher: Elsevier
Journal Title: Biochemical and biophysical research communications
Volume: 488
Issue: 1
Start Page: 81
End Page: 87
Publisher DOI: 10.1016/j.bbrc.2017.05.010
PMID: 28478037
Abstract: STAP-2 is an adaptor molecule regulating several signaling pathways, including TLRs and cytokine/chemokine receptors in immune cells. We previously reported that STAP-2 enhances SDF-1 a-induced Vavl/Racl-mediated T-cell chemotaxis. However, the detailed mechanisms of STAP-2 involvement in enhancing T-cell chemotaxis remain unknown. In the present study, we demonstrate that STAP-2 directly interacts with Pyk2, which is a key molecule in the regulation of SDF-la/CXCR4-mediated T-cell chemotaxis, and increases phosphorylation of Pyk2. Pyk2 itself can induce STAP-2 Y250 phosphorylation, and this phosphorylation is critical for maximal interactions between STAP-2 and Pyk2. Finally, SDF-1 a induced T-cell chemotaxis is inhibited by treatment with Pyk2 siRNA or AG17, an inhibitor of Pyk2, in Jurkat cells overexpressing STAP-2. Taken together, the Pyk2/STAP-2 interaction is a novel mechanism to regulate SDF-1 alpha-dependent T-cell chemotaxis.
Rights: ©2017. This manuscript version is made available under the CC-BY-NC-ND 4.0 license
Type: article (author version)
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: 松田 正

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