| First Author | Schebesta M | Year | 2002 |
| Journal | Immunity | Volume | 17 |
| Issue | 4 | Pages | 473-85 |
| PubMed ID | 12387741 | Mgi Jnum | J:79570 |
| Mgi Id | MGI:2388506 | Doi | 10.1016/s1074-7613(02)00418-1 |
| Citation | Schebesta M, et al. (2002) Control of pre-BCR signaling by Pax5-dependent activation of the BLNK gene. Immunity 17(4):473-85 |
| abstractText | The developmental progression from pro-B to pre-B cells is controlled by pre-B cell receptor (pre-BCR) signaling which depends on BLNK (SLP-65) for coupling the Syk kinase to its downstream effector pathways. Here we identified BLNK as a direct target of the transcription factor Pax5 (BSAP). Restoration of BLNK expression in Ig(mu) transgenic Pax5(-/-) pro-B cells resulted in constitutive pre-BCR signaling and increased cell proliferation without inducing progression to the pre-B cell stage. Ig(mu)(+) Pax5(-/-) pro-B cells expressing a BLNK-estrogen receptor fusion protein initiated signaling immediately upon hormone addition, which facilitated analysis of pre-BCR-induced gene expression changes. The pre-BCR was shown to execute its checkpoint function by regulating genes involved in cell proliferation, intracellular signaling, growth factor responsiveness, and V(D)J recombination. |
