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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 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 Citation Map 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. Related Collections Hematopoiesis and Stem Cells Signal Transduction Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 July 2003, Vol. 102, No. 1, pp. 142-145 HEMATOPOIESIS Brief report 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 From the Department of Pediatrics, Indiana University School of Medicine, Herman B Wells Center for Pediatric Research, Indianapolis; and the Department of Hematology/Pathology, Indiana University School of Medicine, Indianapolis. In vitro studies suggest that activation of class IA phosphatidylinositol 3 (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 (erythroid burst-forming unit [BFU-E]) and late erythroid progenitors (erythroid colony-forming unit [CFU-E]) are reduced in p85-/- fetal livers compared with wild-type 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. (Blood. 2003;102:142-145) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? 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