Adaptor ADAP (adhesion- and degranulation-promoting adaptor protein) regulates β1 integrin clustering on mast cells
被引:11
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作者:
Geng, LP
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机构:Dana Farber Canc Inst, Dept Canc Immunol, Div Tumor Immunol, Boston, MA 02115 USA
Geng, LP
Rudd, C
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机构:
Dana Farber Canc Inst, Dept Canc Immunol, Div Tumor Immunol, Boston, MA 02115 USADana Farber Canc Inst, Dept Canc Immunol, Div Tumor Immunol, Boston, MA 02115 USA
Rudd, C
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机构:
[1] Dana Farber Canc Inst, Dept Canc Immunol, Div Tumor Immunol, Boston, MA 02115 USA
[2] Dana Farber Canc Inst, Dept AIDS, Boston, MA 02115 USA
[3] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA
[4] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA
Aggregation of the high-affinity IgE receptor (FcepsilonRI) activates a tyrosine phosphorylation cascade needed for enhanced adhesion and degranulation events on mast cells. We previously identified the adaptor ADAP (otherwise known as FYB/SLAP) as a modulator of integrin-mediated adhesion of T-cells and mast cells. However, the molecular basis for the effect on beta1 integrin adhesion on mast cells was unclear. In this study, we demonstrate that ADAP can promote the kinetics of beta1 integrin clustering on mast cells. By contrast, the clustering of the FcepsilonRI receptor was unaffected by transfected ADAP, indicating that the promoting effect on clustering was selective for beta1 integrins. These findings extend the modulatory effect of ADAP from beta2 to beta1 members of the integrin family, and provide a molecular basis for the modulatory effect of ADAP on mast cell adhesion. (C) 2001 Elsevier Science.