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http://purl.uniprot.org/citations/10652277http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/10652277http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/10652277http://www.w3.org/2000/01/rdf-schema#comment"Stat5 is activated by multiple receptors of hematopoietic cytokines. To study its role during hematopoiesis, we have generated primary chicken myeloblasts expressing different dominant-negative (dn) alleles of Stat5. This caused a striking inability to generate mature cells, due to massive apoptosis during differentiation. Bcl-2 was able to rescue differentiating cells expressing dnStat5 from apoptosis, suggesting that during cytokine-dependent differentiation the main function of the protein is to ensure cell survival. Our findings with dnStat5-expressing chicken myeloblasts were confirmed with primary hematopoietic cells from Stat5a/Stat5b-deficient mice. Bone marrow cells from these animals displayed a strong increase in apoptotic cell death during GM-CSF-dependent functional maturation in vitro. The antiapoptotic protein Bcl-x was induced by GM-CSF and IL-3 in a Stat5-dependent fashion. Ectopic expression of Bcl-x rescued Stat5-deficient bone marrow cells from apoptosis, indicating that Stat5 promotes the survival of myeloid progenitor cells through its ability to induce transcription of the bcl-x gene. Finally, the recruitment of myeloid cells to inflammatory sites was found strongly impeded in Stat5-deficient mice. Taken together, our findings suggest that Stat5 may promote cytokine-dependent survival and proliferation of differentiating myeloid progenitor cells in stress or pathological situations, such as inflammation."xsd:string
http://purl.uniprot.org/citations/10652277http://purl.uniprot.org/core/author"Decker T."xsd:string
http://purl.uniprot.org/citations/10652277http://purl.uniprot.org/core/author"Decker T."xsd:string
http://purl.uniprot.org/citations/10652277http://purl.uniprot.org/core/author"Beug H."xsd:string
http://purl.uniprot.org/citations/10652277http://purl.uniprot.org/core/author"Beug H."xsd:string
http://purl.uniprot.org/citations/10652277http://purl.uniprot.org/core/author"Hofmann J."xsd:string
http://purl.uniprot.org/citations/10652277http://purl.uniprot.org/core/author"Hofmann J."xsd:string
http://purl.uniprot.org/citations/10652277http://purl.uniprot.org/core/author"Moriggl R."xsd:string
http://purl.uniprot.org/citations/10652277http://purl.uniprot.org/core/author"Moriggl R."xsd:string
http://purl.uniprot.org/citations/10652277http://purl.uniprot.org/core/author"Marine J.C."xsd:string
http://purl.uniprot.org/citations/10652277http://purl.uniprot.org/core/author"Marine J.C."xsd:string
http://purl.uniprot.org/citations/10652277http://purl.uniprot.org/core/author"Ihle J.N."xsd:string
http://purl.uniprot.org/citations/10652277http://purl.uniprot.org/core/author"Ihle J.N."xsd:string
http://purl.uniprot.org/citations/10652277http://purl.uniprot.org/core/author"Kieslinger M."xsd:string
http://purl.uniprot.org/citations/10652277http://purl.uniprot.org/core/author"Kieslinger M."xsd:string
http://purl.uniprot.org/citations/10652277http://purl.uniprot.org/core/author"Woldman I."xsd:string
http://purl.uniprot.org/citations/10652277http://purl.uniprot.org/core/author"Woldman I."xsd:string
http://purl.uniprot.org/citations/10652277http://purl.uniprot.org/core/date"2000"xsd:gYear
http://purl.uniprot.org/citations/10652277http://purl.uniprot.org/core/date"2000"xsd:gYear
http://purl.uniprot.org/citations/10652277http://purl.uniprot.org/core/name"Genes Dev."xsd:string
http://purl.uniprot.org/citations/10652277http://purl.uniprot.org/core/name"Genes Dev"xsd:string
http://purl.uniprot.org/citations/10652277http://purl.uniprot.org/core/pages"232-244"xsd:string
http://purl.uniprot.org/citations/10652277http://purl.uniprot.org/core/pages"232-244"xsd:string