bFGF signaling and v-Myb cooperate in sustained growth of primitive erythroid progenitors

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Item Type:	Article
Title:	bFGF signaling and v-Myb cooperate in sustained growth of primitive erythroid progenitors
Creators Name:	Bartunek, P., Pajer, P., Karafiat, V., Blendinger, G., Dvorak, M. and Zenke, M.
Abstract:	The development of red blood cells from hematopoietic progenitors requires the interplay of specific extracellular factors and transcriptional regulators. Here we have identified an erythroid progenitor that is critically dependent on bFGF and requires expression of AMV v-Myb for sustained proliferation in vitro, indicating that bFGF and Myb proteins cooperate in these cells. In the presence of bFGF such v-Myb cells are completely blocked in their ability to differentiate and exhibit an exceptionally high proliferative potential and long life-span in vitro. Interestingly, in the absence of bFGF cells effectively differentiate into mature erythrocytes, irrespective of constitutive and elevated levels of v-Myb. We also demonstrate that these cells express high levels of FGF receptor type 1 (FGFR1) and that phospholipase C{gamma} (PLCT{gamma}) is one of the important molecules in FGF receptor signaling. Our studies suggest that bFGF, in cooperation with Myb proteins, represents an important factor for determining erythroid lineage choice. These findings unravel a so far unidentified link between extracellular signaling and Myb in hematopoietic cells.
Keywords:	Erythropoiesis, FGF, FGF Receptor, Myb, Signaling, v-Myb
Source:	Oncogene
ISSN:	0950-9232
Publisher:	Nature Publishing Group
Volume:	21
Number:	3
Page Range:	400-410
Date:	17 January 2002
Official Publication:	https://doi.org/10.1038/sj/onc/1205103
PubMed:	View item in PubMed

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