| First Author | Kubo-Akashi C | Year | 2004 |
| Journal | Biochem Biophys Res Commun | Volume | 315 |
| Issue | 2 | Pages | 356-62 |
| PubMed ID | 14766215 | Mgi Jnum | J:88311 |
| Mgi Id | MGI:3032794 | Doi | 10.1016/j.bbrc.2004.01.060 |
| Citation | Kubo-Akashi C, et al. (2004) Roles of a conserved family of adaptor proteins, Lnk, SH2-B, and APS, for mast cell development, growth, and functions: APS-deficiency causes augmented degranulation and reduced actin assembly. Biochem Biophys Res Commun 315(2):356-62 |
| abstractText | Lnk, SH2-B, and APS form a conserved adaptor protein family. All of those proteins are expressed in mast cells and their possible functions in signaling through c-Kit or FcRI have been speculated. To investigate roles of Lnk, SH2-B or APS in mast cells, we established IL-3-dependent mast cells from Ink-/-, SH2-B-/-, and APS -/- mice. IL-3-dependent growth of those cells was comparable. Proliferation or adhesion mediated by c-Kit as well as degranulation induced by cross-linking FcRI were normal in the absence of Lnk or SH2-B. In contrast, APS-deficient mast cells showed augmented degranulation after cross-linking FcRI compared to wild-type cells, while c-Kit-mediated proliferation and adhesion were kept unaffected. APS-deficient mast cells showed reduced actin assembly at steady state, although their various intracellular responses induced by cross-linking FcRI were indistinguishable compared to wild-type cells. Our results suggest potential roles of APS in controlling actin cytoskeleton and magnitude of degranulation in mast cells. |
