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Blood, 1 September 2006, Vol. 108, No. 5, pp. 1524-1532. Prepublished online as a Blood First Edition Paper on May 16, 2006; DOI 10.1182/blood-2005-09-008243. This Article Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2005-09-008243v1 108/5/1524    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Karur, V. G Articles by Wojchowski, D. M Search for Related Content PubMed PubMed Citation Articles by Karur, V. G Articles by Wojchowski, D. M Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted September 9, 2005 Accepted April 21, 2006 LYN kinase promotes erythroblast expansion and late-stage development Vinit G Karur, Clifford A Lowell, Peter Besmer, Valter Agosti, and Don M Wojchowski* Maine Medical Center Research Institute, Scarborough, ME, USA Department of Laboratory Medicine, University of California, San Francisco, CA, USA Sloan-Kettering Institute, New York, NY, USA * Corresponding author; email: wojchd{at}mmc.org. Lyn kinase is known to modulate the formation and function of B-cells, monocytes and mast cells. However, Lyn-/- mice also develop erythro- splenomegaly, and cases for both negative and positive erythropoietic actions of Lyn recently have been outlined. In phenylhydrazine-treated Lyn-/- mice, extramedullary splenic erythropoiesis was hyper-activated, but this did not lead to accelerated recovery from anemia. Furthermore, ex vivo analyses of the development of bone marrow- derived Lyn-/- erythroblasts in unique primary culture systems indicated positive roles for Lyn at two stages. Late stage Lyn-/- erythroblasts exhibited deficit Ter119pos cell formation, and this was paralleled by increased apoptosis (and decreased Bcl-xL expression). During early development, Lyn-/- erythroblasts accumulated at a KitposCD71high stage, possessed decreased proliferative capacity, and were attenuated in entering an apparent G1/S cell cycle phase. In proposed compensatory responses, Lyn-/- erythroblasts expressed increased levels of activated Akt and p60-Src, and decreased levels of death- associated protein kinase-2. Stat5 activation and Bcl-xL expression, in contrast, were significantly decreased in- keeping with decreased survival and developmental potentials. Lyn therefore is proposed to function via erythroid cell- intrinsic mechanisms to promote progenitor cell expansion beyond a KitposCD71high stage, and to support subsequent late-stage development. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D. L. Barber Truth or dare: role of Liar in EPO-dependent signaling Blood, April 16, 2009; 113(16): 3650 - 3651. [Full Text] [PDF] A. L. Samuels, S. P. Klinken, and E. Ingley Liar, a novel Lyn-binding nuclear/cytoplasmic shuttling protein that influences erythropoietin-induced differentiation Blood, April 16, 2009; 113(16): 3845 - 3856. [Abstract] [Full Text] [PDF] C. Dos Santos, C. Demur, V. Bardet, N. Prade-Houdellier, B. Payrastre, and C. Recher A critical role for Lyn in acute myeloid leukemia Blood, February 15, 2008; 111(4): 2269 - 2279. [Abstract] [Full Text] [PDF] P. Sathyanarayana, M. P. Menon, O. Bogacheva, O. Bogachev, K. Niss, W. S. Kapelle, E. Houde, J. Fang, and D. M. Wojchowski Erythropoietin modulation of podocalyxin and a proposed erythroblast niche Blood, July 15, 2007; 110(2): 509 - 518. [Abstract] [Full Text] [PDF]

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