共 8 条
Structural basis for the interaction of the free SH2 domain EAT-2 with SLAM receptors in hematopoietic cells
被引:123
|作者:
Morra, M
[1
]
Lu, J
Poy, F
Martin, M
Sayos, J
Calpe, S
Gullo, C
Howie, D
Rietdijk, S
Thompson, A
Coyle, AJ
Denny, C
Yaffe, MB
Engel, P
Eck, MJ
Terhorst, C
机构:
[1] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Div Immunol, Boston, MA 02115 USA
[2] Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA
[3] Univ Calif Los Angeles, Inst Mol Biol, Los Angeles, CA 90095 USA
[4] Millennium Pharmaceut Inc, Inflammat Div, Cambridge, MA 02139 USA
[5] MIT, Ctr Canc Res, Cambridge, MA 02139 USA
[6] MIT, Dept Biol, Cambridge, MA 02139 USA
[7] Univ Barcelona, Fac Med, Dept Cellular Biol & Pathol, E-08007 Barcelona, Spain
关键词:
antigen-presenting cells;
crystal structure;
EAT-2;
SAP;
XLP;
D O I:
10.1093/emboj/20.21.5840
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
The T and natural killer (NK) cell-specific gene SAP (SH2D1A) encodes a 'free SH2 domain' that binds a specific tyrosine motif in the cytoplasmic tail of SLAM (CD150) and related cell surface proteins. Mutations in SH2D1A cause the X-linked lymphoproliferative disease, a primary immunodeficiency. Here we report that a second gene encoding a free SH2 domain, EAT-2, is expressed in macrophages and B lympho cytes. The EAT-2 structure in complex with a phosphotyrosine peptide containing a sequence motif with Tyr281 of the cytoplasmic tail of CD150 is very similar to the structure of SH2D1A complexed with the same peptide. This explains the high affinity of EAT-2 for the pTyr motif in the cytoplasmic tail of CD150 but, unlike SH2D1A, EAT-2 does not bind to non-phosphorylated CD150. EAT-2 binds to the phosphorylated receptors CD84, CD150, CD229 and CD244, and acts as a natural inhibitor, which interferes with the recruitment of the tyrosine phosphatase SHP-2. We conclude that EAT-2 plays a role in controlling signal transduction through at least four receptors expressed on the surface of professional antigen-presenting cells.
引用
收藏
页码:5840 / 5852
页数:13
相关论文