Open AccessActivation of Stat 5b in erythroid progenitors correlates with the ability of ErbB to induce sustained cell proliferation.
Author(s) -
Georg Mellitzer,
Oliver Wessely,
Thomas Decker,
Andreas Meinke,
Michael J. Hayman,
Hartmut Beug
Publication year - 1996
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.93.18.9600
Subject(s) - erythropoietin receptor , erbb , biology , microbiology and biotechnology , receptor tyrosine kinase , transcription factor , stat , tyrosine phosphorylation , jak stat signaling pathway , phosphorylation , receptor , tyrosine kinase , cancer research , signal transduction , stat3 , gene , biochemistry
Self renewal of normal erythroid progenitors is induced by the receptor tyrosine kinase c-ErbB, whereas other receptors (c-Kit/Epo-R) regulate erythroid differentiation. To address possible mechanisms that could explain this selective activity of c-ErbB, we analyzed the ability of these receptors to activate the different members of the Stat transcription factor family. Ligand activation of c-ErbB induced the tyrosine phosphorylation, DNA-binding, and reporter gene transcription of Stat 5b in erythroblasts. In contrast, ligand activation of c-Kit was unable to induce any of these effects in the same cells. Activation of the erythropoietin receptor caused specific DNA-binding of Stat 5b, but failed to induce reporter gene transcription. These biochemical findings correlate perfectly with the selective ability of c-ErbB to cause sustained self renewal in erythroid progenitors.