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Blood, 15 December 2003, Vol. 102, No. 13, pp. 4354-4360. Prepublished online as a Blood First Edition Paper on August 14, 2003; DOI 10.1182/blood-2003-04-1308. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-04-1308v1 102/13/4354    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 Xu, M.-j. Articles by Zhao, Z. J. Search for Related Content PubMed PubMed Citation Articles by Xu, M.-j. Articles by Zhao, Z. J. Related Collections Signal Transduction Hematopoiesis and Stem Cells Red Cells Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS PTP-MEG2 is activated in polycythemia vera erythroid progenitor cells and is required for growth and expansion of erythroid cells Ming-jiang Xu, Xingwei Sui, Runxiang Zhao, Chunhua Dai, Sanford B. Krantz, and Zhizhuang Joe Zhao From the Hematology/Oncology Division, Department of Medicine, Department of Veterans Affairs Medical Center; and Vanderbilt-Ingram Cancer Center, Vanderbilt University, Nashville, TN. Polycythemia vera (PV) is a human clonal hematologic disorder. Previously we demonstrated that erythroid colony-forming cells (ECFCs) from PV patients contained a hyperactive membrane-associated tyrosine phosphatase. We now show that this phosphatase corresponded to protein tyrosine phosphatase (PTP)-MEG2, an intracellular enzyme with a putative lipid-binding domain. The increased activity of PTP-MEG2 in PV cells is due to its elevated distribution in the membrane fraction. With the development of ECFCs to mature red cells, the protein level of PTP-MEG2 decreased gradually, but membrane-associated PTP-MEG2 was sustained for a longer period of time in PV cells, which correlated with an enhanced colony-forming capability of the cells. Importantly, expression of dominant-negative mutant forms of PTP-MEG2 suppressed in vitro growth and expansion of both normal and PV ECFCs. The data indicate that PTP-MEG2 has an important role in the development of erythroid cells. (Blood. 2003;102:4354-4360) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. Zeuner, F. Pedini, M. Signore, G. Ruscio, C. Messina, A. Tafuri, G. Girelli, C. Peschle, and R. De Maria Increased death receptor resistance and FLIPshort expression in polycythemia vera erythroid precursor cells Blood, May 1, 2006; 107(9): 3495 - 3502. [Abstract] [Full Text] [PDF] R. Zhao, S. Xing, Z. Li, X. Fu, Q. Li, S. B. Krantz, and Z. J. Zhao Identification of an Acquired JAK2 Mutation in Polycythemia Vera J. Biol. Chem., June 17, 2005; 280(24): 22788 - 22792. [Abstract] [Full Text] [PDF] M.-Z. Zhang, W. Mai, C. Li, S.-y. Cho, C. Hao, G. Moeckel, R. Zhao, I. Kim, J. Wang, H. Xiong, et al. PKHD1 protein encoded by the gene for autosomal recessive polycystic kidney disease associates with basal bodies and primary cilia in renal epithelial cells PNAS, February 24, 2004; 101(8): 2311 - 2316. [Abstract] [Full Text] [PDF]

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