ARAP, a novel adaptor protein, is required for TCR signaling and integrin-mediated adhesion
- 등재 SCIE, SCOPUS
- 발행기관 American Association of Immunologists
- 발행년도 2016
- 총서유형 Journal
- URI http://www.dcollection.net/handler/ewha/000000135307
- 본문언어 영어
- Published As http://dx.doi.org/10.4049/jimmunol.1501913
- 저작권 이화여자대학교 논문은 저작권에 의해 보호받습니다.
초록/요약
A novel adaptor protein was identified by analyzing phosphotyrosine proteomes from membrane rafts of activated T cells. This protein showed sequence similarity to a well-known T cell adaptor protein, adhesion and degranulation-promoting adaptor protein (ADAP); therefore, the novel protein was designated activation-dependent, raft-recruited ADAP-like phosphoprotein (ARAP). Suppression of ARAP impaired the major signaling pathways downstream of the TCR. ARAP associated with the Src homology 2 domain of Src homology 2-containing leukocyte protein of 76 kDa via the phosphorylation of two YDDV motifs in response to TCR stimulation. ARAP also mediated integrin activation but was not involved in actin polymerization. The results of this study indicate that a novel T cell adaptor protein, ARAP, plays a unique role in T cells as a part of both the proximal activation signaling and inside-out signaling pathways that result in integrin activation and T cell adhesion. Copyright © 2016 by The American Association of Immunologists, Inc.
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