| First Author | Fruman DA | Year | 1999 |
| Journal | Science | Volume | 283 |
| Issue | 5400 | Pages | 393-7 |
| PubMed ID | 9888855 | Mgi Jnum | J:52229 |
| Mgi Id | MGI:1328662 | Doi | 10.1126/science.283.5400.393 |
| Citation | Fruman DA, et al. (1999) Impaired B cell development and proliferation in absence of phosphoinositide 3-kinase p85alpha. Science 283(5400):393-7 |
| abstractText | Phosphoinositide 3-kinase (PI3K) activation has been implicated in many cellular responses, including fibroblast growth, transformation, survival, and chemotaxis. Although PI3K is activated by several agents that stimulate T and B cells, the role of PI3K in lymphocyte function is not clear. The mouse gene encoding the PI3K adapter subunit p85alpha and its splice variants p55alpha and p50alpha was disrupted. Most p85alpha-p55alpha-p50alpha-/- mice die within days after birth. Lymphocyte development and function was studied with the use of the RAG2-deficient blastocyst complementation system. Chimeric mice had reduced numbers of peripheral mature B cells and decreased serum immunoglobulin. The B cells that developed had diminished proliferative responses to antibody to immunoglobulin M, antibody to CD40, and lipopolysaccharide stimulation and decreased survival after incubation with interleukin-4. In contrast, T cell development and proliferation was normal. This phenotype is similar to defects observed in mice lacking the tyrosine kinase Btk. |
