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Prepublished online as a Blood First Edition Paper on March 6, 2003; DOI 10.1182/blood-2002-10-3245. This Article Full Text (PDF) All Versions of this Article: 2002-10-3245v1 102/1/142    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 Huddleston, H. Articles by Ingram, D. A Search for Related Content PubMed PubMed Citation Articles by Huddleston, H. Articles by Ingram, D. A Social Bookmarking                   What's this? Submitted October 25, 2002 Accepted February 21, 2003 A functional p85 gene is required for normal murine fetal erythropoiesis Hannah Huddleston, Bailin Tan, Feng-Chun Yang, Hilary White, Mary Jo Wenning, Attilio Orazi, Mervin C Yoder, Reuben Kapur, and David A Ingram* Department of Pediatrics, Indiana University School of Medicine, Herman B Wells Center for Pediatric Research, Indianapolis, IN, USA Department of Hematology/Pathology, Indiana University School of Medicine, Indianapolis, IN, USA * Corresponding author; email: dingram{at}iupui.edu. In vitro studies suggest that activation of class IA PI-3 kinase is necessary for normal erythroid cell development. However, when class IA PI-3 kinase deficient mice were generated by a targeted deletion of the p85 regulatory subunit, fetal erythropoiesis was reportedly unaffected. Given the discrepancies between these studies, we performed a more detailed in vivo analysis of class IA PI-3 kinase deficient embryos. Day 14.5 p85 -/- embryos are pale with a marked reduction of mature erythrocytes in their peripheral blood. Further, the absolute number and frequency of both early (BFU-E) and late erythroid progenitors (CFU-E) are reduced in p85 -/- fetal livers compared to wildtype controls, which is associated with reduced proliferation. Taken together, these data establish an important role for p85 and class IA PI-3 kinase in regulating the development of both early and late erythroid progenitors in fetal liver. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: Y. Zhang, E. Diaz-Flores, G. Li, Z. Wang, Z. Kang, E. Haviernikova, S. Rowe, C.-K. Qu, W. Tse, K. M. Shannon, et al. Abnormal hematopoiesis in Gab2 mutant mice Blood, July 1, 2007; 110(1): 116 - 124. [Abstract] [Full Text] [PDF] W. J. Bakker, T. B. van Dijk, M. Parren-van Amelsvoort, A. Kolbus, K. Yamamoto, P. Steinlein, R. G. W. Verhaak, T. W. Mak, H. 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