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Blood, 15 June 2006, Vol. 107, No. 12, pp. 4754-4762. Prepublished online as a Blood First Edition Paper on March 2, 2006; DOI 10.1182/blood-2006-01-0141. This Article Full Text Full Text (PDF) Supplemental Table and Figures All Versions of this Article: 2006-01-0141v1 107/12/4754    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 Bäumer, S. Articles by Vestweber, D. Search for Related Content PubMed PubMed Citation Articles by Bäumer, S. Articles by Vestweber, D. Related Collections Hemostasis, Thrombosis, and Vascular Biology Signal Transduction Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Vascular endothelial cell–specific phosphotyrosine phosphatase (VE-PTP) activity is required for blood vessel development Sebastian Bäumer, Linda Keller, Astrid Holtmann, Ruth Funke, Benjamin August, Alexander Gamp, Hartwig Wolburg, Karen Wolburg-Buchholz, Urban Deutsch, and Dietmar Vestweber From the Max-Planck-Institute of Molecular Biomedicine, Münster, Germany; the Theodor-Kocher-Institute, University of Bern, Switzerland; and the Institute of Pathology, University of Tübingen, Germany. VE-PTP, a receptor-type phosphotyrosine phosphatase, associates with the tyrosine kinase receptor Tie-2 and VE-cadherin and enhances the adhesive function of the latter. Here, VE-PTP was found to be restricted to endothelial cells, with a preference for arterial endothelium. Mutant mice expressing a truncated, secreted form of VE-PTP lacking the cytoplasmic and transmembrane domains and the most membrane-proximal extracellular fibronectin type III repeat, showed severe vascular malformations causing lethality at 10 days of gestation. Although blood vessels were initially formed, the intraembryonic vascular system soon deteriorated. Blood vessels in the yolk sac developed into dramatically enlarged cavities. In explant cultures of mutant allantoides, endothelial cells were found next to vessel structures growing as cell layers. No signs for enhanced endothelial apoptosis or proliferation were observed. Thus, the activity of VE-PTP is not required for the initial formation of blood vessels, yet it is essential for their maintenance and remodeling. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: PTPs seize the spotlight from RTKs in vasculogenesis Christopher J. Drake and W. Scott Argraves Blood 2006 107: 4582. [Full Text] [PDF] This article has been cited by other articles: M. Winderlich, L. Keller, G. Cagna, A. Broermann, O. Kamenyeva, F. Kiefer, U. Deutsch, A. F. Nottebaum, and D. Vestweber VE-PTP controls blood vessel development by balancing Tie-2 activity J. Cell Biol., May 18, 2009; 185(4): 657 - 671. [Abstract] [Full Text] [PDF] S. Mellberg, A. Dimberg, F. Bahram, M. Hayashi, E. Rennel, A. Ameur, J. O. Westholm, E. Larsson, P. Lindahl, M. J. Cross, et al. Transcriptional profiling reveals a critical role for tyrosine phosphatase VE-PTP in regulation of VEGFR2 activity and endothelial cell morphogenesis FASEB J, May 1, 2009; 23(5): 1490 - 1502. [Abstract] [Full Text] [PDF] H. Sadakata, H. Okazawa, T. Sato, Y. Supriatna, H. Ohnishi, S. Kusakari, Y. Murata, T. Ito, U. Nishiyama, T. Minegishi, et al. SAP-1 is a microvillus-specific protein tyrosine phosphatase that modulates intestinal tumorigenesis Genes Cells, March 1, 2009; 14(3): 295 - 308. [Abstract] [Full Text] [PDF] A. F. Nottebaum, G. Cagna, M. Winderlich, A. C. Gamp, R. Linnepe, C. Polaschegg, K. Filippova, R. Lyck, B. Engelhardt, O. Kamenyeva, et al. VE-PTP maintains the endothelial barrier via plakoglobin and becomes dissociated from VE-cadherin by leukocytes and by VEGF J. Exp. Med., November 24, 2008; 205(12): 2929 - 2945. [Abstract] [Full Text] [PDF] E. Dejana, F. Orsenigo, and M. G. Lampugnani The role of adherens junctions and VE-cadherin in the control of vascular permeability J. Cell Sci., July 1, 2008; 121(13): 2115 - 2122. [Abstract] [Full Text] [PDF] T. Katsuno, K. Umeda, T. Matsui, M. Hata, A. Tamura, M. Itoh, K. Takeuchi, T. Fujimori, Y.-i. Nabeshima, T. Noda, et al. Deficiency of Zonula Occludens-1 Causes Embryonic Lethal Phenotype Associated with Defected Yolk Sac Angiogenesis and Apoptosis of Embryonic Cells Mol. Biol. Cell, June 1, 2008; 19(6): 2465 - 2475. [Abstract] [Full Text] [PDF] D. Vestweber VE-Cadherin: The Major Endothelial Adhesion Molecule Controlling Cellular Junctions and Blood Vessel Formation Arterioscler Thromb Vasc Biol, February 1, 2008; 28(2): 223 - 232. [Abstract] [Full Text] [PDF] M. Affara, B. Dunmore, C. Savoie, S. Imoto, Y. Tamada, H. Araki, D. S. Charnock-Jones, S. Miyano, and C. Print Understanding endothelial cell apoptosis: what can the transcriptome, glycome and proteome reveal? Phil Trans R Soc B, August 29, 2007; 362(1484): 1469 - 1487. [Abstract] [Full Text] [PDF] M. G. Dominguez, V. C. Hughes, L. Pan, M. Simmons, C. Daly, K. Anderson, I. Noguera-Troise, A. J. Murphy, D. M. Valenzuela, S. Davis, et al. Vascular endothelial tyrosine phosphatase (VE-PTP)-null mice undergo vasculogenesis but die embryonically because of defects in angiogenesis PNAS, February 27, 2007; 104(9): 3243 - 3248. [Abstract] [Full Text] [PDF]

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