| First Author | Ono M | Year | 1997 |
| Journal | Cell | Volume | 90 |
| Issue | 2 | Pages | 293-301 |
| PubMed ID | 9244303 | Mgi Jnum | J:41976 |
| Mgi Id | MGI:894891 | Doi | 10.1016/s0092-8674(00)80337-2 |
| Citation | Ono M, et al. (1997) Deletion of SHIP or SHP-1 reveals two distinct pathways for inhibitory signaling. Cell 90(2):293-301 |
| abstractText | Two signaling molecules have been implicated in the modulation of immune receptor activation by inhibitory coreceptors: an inositol polyphosphate 5'-phosphatase, SHIP, and a tyrosine phosphatase, SHP-1. To address the necessity, interaction, or redundancy of these signaling molecules, we have generated SHP-1- or SHIP-deficient B cell lines and determined their ability to mediate inhibitory signaling. Two distinct classes of inhibitory responses are defined, mediated by the selective recruitment of SHP-1 or SHIP. The Fc gammaRIIB class of inhibitory signaling is dependent on SHIP and not SHP-1; conversely, the KIR class requires SHP-1 and not SHIP. The consequence of this selective recruitment by inhibitory receptor engagement is seen in BCR-triggered apoptosis. SHP-1-mediated inhibitory signaling blocks apoptosis, while SHIP recruitment attenuates a proapoptotic signal initiated by Fc gammaRIIB. |
