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Blood, 15 July 2006, Vol. 108, No. 2, pp. 591-599. Prepublished online as a Blood First Edition Paper on March 28, 2006; DOI 10.1182/blood-2005-11-4616. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: 2005-11-4616v1 108/2/591    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 Schnell, S. Articles by Jacobs, H. Search for Related Content PubMed PubMed Citation Articles by Schnell, S. Articles by Jacobs, H. Related Collections Apoptosis Signal Transduction Immunobiology Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Gimap4 accelerates T-cell death Silke Schnell, Corinne Démollière, Paul van den Berk, and Heinz Jacobs From the Division of Immunology, The Netherlands Cancer Institute, Amsterdam; and Department of Immunology, University of Basel, Switzerland. Gimap4, a member of the newly identified GTPase of the immunity-associated protein family (Gimap), is strongly induced by the pre–T-cell receptor in precursor T lymphocytes, transiently shut off in double-positive thymocytes, and reappears after TCR-mediated positive selection. Here, we show that Gimap4 remains expressed constitutively in the cytosol of mature T cells. A C-terminal IQ domain binds calmodulin in the absence of calcium, and conserved PKC phosphorylation motifs are targets of concanavalin A (ConA)– or PMA/ionomycin-induced PKC activation. To address the role of Gimap4 in T-cell physiology, we completed the genomic organization of the gimap4 locus and generated a Gimap4-null mutant mouse. Studies in these mice revealed no critical role of Gimap4 in T-cell development but in the regulation of apoptosis. We have found that Gimap4 accelerates the execution of programmed cell death induced by intrinsic stimuli downstream of caspase-3 activation and phosphatidylserine exposure. Apoptosis directly correlates with the phosphorylation status of Gimap4. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Per aspera ad astra: from early T-cell development to accelerating late T-cell apoptosis Henning Walczak Blood 2006 108: 410. [Full Text] [PDF] This article has been cited by other articles: K. A. Duthie, L. C. Osborne, L. J. Foster, and N. Abraham Proteomics Analysis of Interleukin (IL)-7-induced Signaling Effectors Shows Selective Changes in IL-7R{alpha}449F Knock-in T Cell Progenitors Mol. Cell. Proteomics, October 1, 2007; 6(10): 1700 - 1710. [Abstract] [Full Text] [PDF] C. Carter, C. Dion, S. Schnell, W. J. Coadwell, M. Graham, L. Hepburn, G. Morgan, A. Hutchings, J. C. Pascall, H. Jacobs, et al. A Natural Hypomorphic Variant of the Apoptosis Regulator Gimap4/IAN1 J. Immunol., August 1, 2007; 179(3): 1784 - 1795. [Abstract] [Full Text] [PDF] T. A. Baldwin and K. A. Hogquist Transcriptional Analysis of Clonal Deletion In Vivo J. Immunol., July 15, 2007; 179(2): 837 - 844. [Abstract] [Full Text] [PDF] U. Dalberg, H. Markholst, and L. Hornum Both Gimap5 and the diabetogenic BBDP allele of Gimap5 induce apoptosis in T cells Int. Immunol., April 1, 2007; 19(4): 447 - 453. [Abstract] [Full Text] [PDF]

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