Related Experiment Video
Updated: Aug 4, 2026
Transduction-Transplantation Mouse Model of Myeloproliferative Neoplasm
Published on: December 22, 2016
Transgenic bcl-2 is not sufficient to rescue all hematolymphoid defects in STAT5A/5B-deficient mice
Jonathan W Snow1, Ninan Abraham, Melissa C Ma
1Gladstone Institute of Virology and Immunology, Department of Microbiology and Immunology, University of California at San Francisco, San Francisco, CA 94141-9100, USA.
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.
