| First Author | Saitoh S | Year | 2000 |
| Journal | Immunity | Volume | 12 |
| Issue | 5 | Pages | 525-35 |
| PubMed ID | 10843385 | Mgi Jnum | J:111435 |
| Mgi Id | MGI:3653988 | Doi | 10.1016/s1074-7613(00)80204-6 |
| Citation | Saitoh S, et al. (2000) LAT is essential for Fc(epsilon)RI-mediated mast cell activation. Immunity 12(5):525-35 |
| abstractText | The linker molecule LAT is a substrate of the tyrosine kinases activated following TCR engagement of T cells. LAT is also expressed in platelets, NK, and mast cells. Although LAT-deficient mice contain normal numbers of mast cells, we found that LAT-deficient mice were resistant to IgE-mediated passive systemic anaphylaxis. LAT-deficient bone marrow-derived mast cells (BMMC) showed normal growth and development. Whereas tyrosine phosphorylation of Fc(epsilon)RI, Syk, and Vav was intact in LAT-deficient BMMCs following Fc(epsilon)RI engagement, tyrosine phosphorylation of SLP-76, PLC-gamma1, and PLC-gamma2 and calcium mobilization were dramatically reduced. LAT-deficient BMMCs also exhibited profound defects in activation of MAPK, degranulation, and cytokine production after Fc(epsilon)RI cross-linking. These results show that LAT plays a critical role in Fc(epsilon)RI-mediated signaling in mast cells. |
