| First Author | Snow JW | Year | 2003 |
| Journal | Exp Hematol | Volume | 31 |
| Issue | 12 | Pages | 1253-8 |
| PubMed ID | 14662332 | Mgi Jnum | J:115667 |
| Mgi Id | MGI:3692054 | Doi | 10.1016/j.exphem.2003.09.014 |
| Citation | Snow JW, et al. (2003) Transgenic bcl-2 is not sufficient to rescue all hematolymphoid defects in STAT5A/5B-deficient mice. Exp Hematol 31(12):1253-8 |
| abstractText | OBJECTIVE: Cytokines bind high-affinity receptors expressed on hematopoietic cells to initiate signaling cascades that regulate differentiation, proliferation, and survival. Previous studies have established a role for STAT5 in transducing survival signals for hematopoietic progenitor cells in response to cytokines. MATERIALS AND METHODS: To determine if constitutive expression of a member of the bcl-2 family of anti-apoptotic proteins could compensate for the loss of STAT5, we utilized combinatorial genetics to generate STAT5A/5B-deficient mice expressing a bcl-2 transgene. RESULTS: Although bcl-2 expression restored peripheral blood counts to normal in STAT5A/5B(-/-) mice, we noted a striking failure of this transgene to correct defects in hematopoietic stem and progenitor cells. CONCLUSION: These data imply important effects of STAT5 in modulating hematopoietic cells in addition to promoting survival per se. |
