| First Author | Suzuki H | Year | 2003 |
| Journal | Nat Immunol | Volume | 4 |
| Issue | 3 | Pages | 280-6 |
| PubMed ID | 12563258 | Mgi Jnum | J:96704 |
| Mgi Id | MGI:3531269 | Doi | 10.1038/ni890 |
| Citation | Suzuki H, et al. (2003) PI3K and Btk differentially regulate B cell antigen receptor-mediated signal transduction. Nat Immunol 4(3):280-6 |
| abstractText | Phosphoinositide-3 kinase (PI3K) is thought to activate the tyrosine kinase Btk. However, through analysis of PI3K-/- and Btk-/- mice, B cell antigen receptor (BCR)-induced activation of Btk in mouse B cells was found to be unaffected by PI3K inhibitors or by a lack of PI3K. Consistent with this observation, PI3K-/- Btk-/- double-deficient mice had more severe defects than either single-mutant mouse. NF-kappaB activation along with Bcl-xL and cyclin D2 induction were severely blocked in both PI3K-/- and Btk-/- single-deficient B cells. Transgenic expression of Bcl-xL restored the development and BCR-induced proliferation of B cells in PI3K-/- mice. Our results indicate that PI3K and Btk have unique roles in proximal BCR signaling and that they have a common target further downstream in the activation of NF-kappaB. |
