Transgenic bcl-2 is not sufficient to rescue all hematolymphoid defects in STAT5A/5B-deficient mice

Jonathan W. Snow, Ninan Abraham, Melissa C. Ma, Sarah K. Bronson, Mark A. Goldsmith

Research output: Contribution to journalArticle

11 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1253-1258
Number of pages6
JournalExperimental Hematology
Volume31
Issue number12
DOIs
StatePublished - Dec 2003

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Hematology
  • Genetics
  • Cell Biology
  • Cancer Research

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