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This Article Full Text Full Text (PDF) 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 Carballo, E. Articles by Blackshear, P. J. Search for Related Content PubMed PubMed Citation Articles by Carballo, E. Articles by Blackshear, P. J. Related Collections Hematopoiesis and Stem Cells Gene Expression Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 October 2001, Vol. 98, No. 8, pp. 2389-2395 HEMATOPOIESIS Roles of tumor necrosis factor- receptor subtypes in the pathogenesis of the tristetraprolin-deficiency syndrome Ester Carballo and Perry J. Blackshear From the Office of Clinical Research and Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, Research Triangle Park, NC; and Departments of Medicine and Biochemistry, Duke University Medical Center, Durham, NC. Tristetraprolin (TTP) is a member of the CCCH tandem zinc-finger class of proteins. It can bind to and destabilize mRNAs encoding tumor necrosis factor- (TNF-) and granulocyte-macrophage colony-stimulating factor (GM-CSF). Conversely, mice deficient in TTP develop a complex syndrome characterized by cachexia, myeloid hyperplasia, and joint and skin inflammation. Studies using anti-TNF- neutralizing antibodies demonstrated that this syndrome, at least in part, is a consequence of the excess production of TNF- in the absence of TTP. To evaluate the role played by each TNF- receptor in the pathogenesis of this syndrome, mice were generated that were deficient in TTP and either or both of the known TNF- receptors (TNFRs), type 1 (TNFR1) and type 2 (TNFR2). Mice deficient in TTP and TNFR1, or in TTP and both receptors, were protected from developing the TNF--induced cachexia and inflammation. In contrast, mice deficient in TNFR2 were more severely affected than mice deficient in TTP alone, suggesting that TNFR2 might play a protective role in the development of the syndrome. In cultured cells derived from these mice, apparent cooperation between the TNFRs was required to achieve normal TNF--induced expression of TTP, TNF-, and GM-CSF mRNAs. Finally, the results showed that TNFR1 plays an important role in mediating TNF--induced changes in TNF- and GM-CSF mRNA stability. © 2001 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. M. S. Hartz, B. Bauer, M. L. Block, J.-S. Hong, and D. S. Miller Diesel exhaust particles induce oxidative stress, proinflammatory signaling, and P-glycoprotein up-regulation at the blood-brain barrier FASEB J, August 1, 2008; 22(8): 2723 - 2733. [Abstract] [Full Text] [PDF] W. S. Lai, J. S. Parker, S. F. Grissom, D. J. Stumpo, and P. J. Blackshear Novel mRNA Targets for Tristetraprolin (TTP) Identified by Global Analysis of Stabilized Transcripts in TTP-Deficient Fibroblasts Mol. Cell. Biol., December 15, 2006; 26(24): 9196 - 9208. [Abstract] [Full Text] [PDF] D. J. Stumpo, N. A. Byrd, R. S. Phillips, S. Ghosh, R. R. Maronpot, T. Castranio, E. N. Meyers, Y. Mishina, and P. J. Blackshear Chorioallantoic Fusion Defects and Embryonic Lethality Resulting from Disruption of Zfp36L1, a Gene Encoding a CCCH Tandem Zinc Finger Protein of the Tristetraprolin Family Mol. Cell. Biol., July 15, 2004; 24(14): 6445 - 6455. 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