| First Author | Abraham N | Year | 2005 |
| Journal | Oncogene | Volume | 24 |
| Issue | 33 | Pages | 5252-7 |
| PubMed ID | 15870688 | Mgi Jnum | J:100190 |
| Mgi Id | MGI:3587464 | Doi | 10.1038/sj.onc.1208726 |
| Citation | Abraham N, et al. (2005) Haploinsufficiency identifies STAT5 as a modifier of IL-7-induced lymphomas. Oncogene 24(33):5252-7 |
| abstractText | The requirement for receptor components and the signalling effector, signal transducer and activator of transcription (STAT) 5A/5B, was assessed genetically in a lymphoma development model induced by interleukin-7 (IL-7). This growth factor for T- and B-cell progenitors and mature lymphocytes activates survival and proliferative pathways including Bcl-2, phosphatidylinositol-3 kinase and STAT5. Overexpression of IL-7 in vivo causes early mortality from lymphoma development. Mice overexpressing IL-7 that were heterozygous for the IL-7Ralpha subunit showed improved survival compared to wild-type mice. In addition, STAT5A/5B+/- compound heterozygous mice with one targeted allele each of STAT5A and STAT5B showed striking amelioration of IL-7-induced mortality and disease development. STAT5A/5B+/- compound heterozygous mice were otherwise normal in stem cell and lymphocyte development and cellularity. Lower STAT5 protein levels accompanied the reduction in STAT5A/5B copy number, which suggests that STAT5 haploinsufficiency is a modifier of IL-7 signal strength. |
