| First Author | Yamanashi Y | Year | 2000 |
| Journal | Genes Dev | Volume | 14 |
| Issue | 1 | Pages | 11-6 |
| PubMed ID | 10640270 | Mgi Jnum | J:95641 |
| Mgi Id | MGI:3526675 | Doi | 10.1101/gad.14.1.11 |
| Citation | Yamanashi Y, et al. (2000) Role of the rasGAP-associated docking protein p62(dok) in negative regulation of B cell receptor-mediated signaling. Genes Dev 14(1):11-6 |
| abstractText | Antigenic stimulation of the B-cell receptor (BCR) is a central event in the immune response. In contrast, antigen bound to IgG negatively regulates signals from the BCR by cross-linking it to the inhibitory receptor FcgammaRIIB. Here we show that upon cross-linking of BCR or BCR with FcgammaRIIB, the rasGAP-associated protein p62(dok) is prominently tyrosine phosphorylated in a Lyn-dependent manner. Inactivation of the dok gene by homologous recombination has shown that upon BCR cross-linking, p62(dok) suppresses MAP kinase and is indispensable for FcgammaRIIB-mediated negative regulation of cell proliferation. We propose that p62(dok), a downstream target of many PTKs, plays a negative role in various signaling situations. |
