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Blood, 26 February 2009, Vol. 113, No. 9, pp. 1919-1928. Prepublished online as a Blood First Edition Paper on December 24, 2008; DOI 10.1182/blood-2008-06-159574. This Article Full Text (PDF) Supplemental Tables and Figure All Versions of this Article: blood-2008-06-159574v1 113/9/1919    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 Praetor, A. Articles by Fong, S. Search for Related Content PubMed PubMed Citation Articles by Praetor, A. Articles by Fong, S. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted June 13, 2008 Accepted November 7, 2008 Genetic deletion of JAM-C reveals a role in myeloid progenitor generation Asja Praetor*, Jacqueline M. McBride, Henry Chiu, Linda Rangell, Lorena Cabote, Wyne P. Lee, James Cupp, Dimitry M. Danilenko, and Sherman Fong Department of Immunology, Genentech, Inc., South San Francisco, CA, United States Department of Pathology, Genentech, Inc., South San Francisco, CA, United States * Corresponding author; email: praetor_asja{at}lilly.com. Hematopoietic stem cells (HSC) have the capacity to self-renew and continuously differentiate into all blood cell lineages throughout life. At each branching point during differentiation interactions with the environment are key in the generation of daughter cells with distinct fates. Here we examined the role of the cell adhesion molecule JAM-C, a protein known to mediate cellular polarity during spermatogenesis, in hematopoiesis. We show that murine JAM-C is highly expressed on HSCs in the bone marrow (BM). Expression correlates with self-renewal, being highest on long-term repopulating HSCs, and decreases with differentiation, being maintained longest among myeloid committed progenitors. Inclusion of JAM-C as a sole marker on lineage negative BM cells yields HSC enrichments and long-term multi-lineage reconstitution when transferred to lethally irradiated mice. Analysis of Jam-C deficient mice showed that two-thirds die within 48 hours after birth. In the surviving animals loss of Jam-C leads to an increase in myeloid progenitors and granulocytes in the BM. Stem cells and myeloid cells from fetal liver are normal in number and homing to the BM. These results provide evidence that JAM-C defines HSCs in the BM and that JAM-C plays a role in controlling myeloid progenitor generation in the BM. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. Scheiermann, B. Colom, P. Meda, N. S.A. Patel, M.-B. Voisin, A. Marrelli, A. Woodfin, C. Pitzalis, C. Thiemermann, M. Aurrand-Lions, et al. Junctional Adhesion Molecule-C Mediates Leukocyte Infiltration in Response to Ischemia Reperfusion Injury Arterioscler Thromb Vasc Biol, October 1, 2009; 29(10): 1509 - 1515. [Abstract] [Full Text] [PDF]

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