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Prepublished online as a Blood First Edition Paper on November 14, 2002; DOI 10.1182/blood-2002-07-2250. This Article Full Text (PDF) All Versions of this Article: 2002-07-2250v1 101/6/2250    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 Aiyagari, A. L Articles by Shannon, K. M Search for Related Content PubMed PubMed Citation Articles by Aiyagari, A. L Articles by Shannon, K. M Social Bookmarking                   What's this? Submitted July 25, 2002 Accepted November 2, 2002 Hematologic effects of inactivating the Ras processing enzyme Rce1 Abigail L Aiyagari, Brigit R Taylor, Vikas Aurora, Stephen G Young, and Kevin M Shannon* Department of Pediatrics, UCSF, San Francisco, CA, USA Department of Medicine, UCSF, San Francisco, CA, USA * Corresponding author; email: kevins{at}itsa.ucsf.edu. Post-translational processing of Ras proteins has attracted considerable interest as a potential target for anticancer drug discovery. Rce1 encodes an endoprotease that facilitates membrane targeting of Ras and other prenylated proteins by releasing the carboxyl-terminal three amino acids (i.e., the AAX of the CAAX motif). Homozygous Rce1 mutant embryos (Rce1-/-) die late in gestation. To characterize the role of Rce1 in hematopoiesis, we performed adoptive transfers and investigated cells from the recipients. Rce1-/- fetal liver cells rescued lethally irradiated recipients and manifested normal long-term repopulating potential in competitive repopulation assays. The recipients of Rce1-/- cells developed modest elevations in mature myeloid cells (neutrophils + monocytes), but remained well. Bone marrow cells from mice transplanted with Rce1-/- activated ERK kinase normally in response to granulocyte macrophage colony stimulating factor. These data suggest that pharmacologic inhibitors of Rce1 will have minimal effects on normal hematopoietic cells. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. M. Wahlstrom, B. A. Cutts, M. Liu, A. Lindskog, C. Karlsson, A.-K. M. Sjogren, K. M. E. Andersson, S. G. Young, and M. O. Bergo Inactivating Icmt ameliorates K-RAS-induced myeloproliferative disease Blood, August 15, 2008; 112(4): 1357 - 1365. [Abstract] [Full Text] [PDF] C. Flotho, C. P. Kratz, and C. M. Niemeyer How a rare pediatric neoplasia can give important insights into biological concepts: a perspective on juvenile myelomonocytic leukemia Haematologica, November 1, 2007; 92(11): 1441 - 1446. [Full Text] [PDF] A. M. Wahlstrom, B. A. Cutts, C. Karlsson, K. M. E. Andersson, M. Liu, A.-K. M. Sjogren, B. Swolin, S. G. Young, and M. O. Bergo Rce1 deficiency accelerates the development of K-RAS-induced myeloproliferative disease Blood, January 15, 2007; 109(2): 763 - 768. [Abstract] [Full Text] [PDF] F. Fueller, M. O. Bergo, S. G. Young, K. Aktories, and G. Schmidt Endoproteolytic Processing of RhoA by Rce1 Is Required for the Cleavage of RhoA by Yersinia enterocolitica Outer Protein T Infect. Immun., March 1, 2006; 74(3): 1712 - 1717. [Abstract] [Full Text] [PDF] M. O. Bergo, H. D. Lieu, B. J. Gavino, P. Ambroziak, J. C. Otto, P. J. Casey, Q. M. Walker, and S. G. Young On the Physiological Importance of Endoproteolysis of CAAX Proteins: HEART-SPECIFIC RCE1 KNOCKOUT MICE DEVELOP A LETHAL CARDIOMYOPATHY J. Biol. Chem., February 6, 2004; 279(6): 4729 - 4736. [Abstract] [Full Text] [PDF]

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