Effect of Tyrosine Kinase on TCR-Mediated Activation of Integrin
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- ITSUSAKI Hiroshi
- Department of Biochemistry, Osaka Dental University, Osaka, Japan
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- GODA Seiji
- Department of Biochemistry, Osaka Dental University, Osaka, Japan
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- KAMADA Aiko
- Department of Biochemistry, Osaka Dental University, Osaka, Japan
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- IKEO Takashi
- Department of Biochemistry, Osaka Dental University, Osaka, Japan
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抄録
Stimulation of the CD3/TCR results within minutes in an increase in T cell adhesion to fibronectin. The biochemical pathways that control TCR-mediated increases in adhesion to fibronectin remain poorly characterized. In this study, the role of the tyrosine kinase in the regulation of adhesion by the CD3/TCR was investigated. CD3 stimulation enhanced adhesion to fibronectin on Jurkat T cells line. Tyrosine kinase inhibitor, PP2, and anti β1 integrin mAb blocked adhesion to fibronectin enhanced by CD3 stimulation on Jurkat T cells. CD3 stimulation did not increase adhesion to fibronectin of the tyrosine kinase ZAP-70-deficient Jurkat T cells line, P116. Furthermore, CD3 stimulation failed to tyrosine phosphorylation of PI3-kinase enzyme AKT on P116 cells. These observations support a model in which the tyrosine kinase activity of ZAP-70 kinase is critical for regulation of β1 integrin activity by CD3/TCR.
収録刊行物
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- Journal of Oral Tissue Engineering
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Journal of Oral Tissue Engineering 7 (2), 81-88, 2009
日本再生歯科医学会
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詳細情報 詳細情報について
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- CRID
- 1390001205226064640
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- NII論文ID
- 130004456609
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- ISSN
- 18800823
- 13489623
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可