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Blood, 1 February 2005, Vol. 105, No. 3, pp. 1187-1194. Prepublished online as a Blood First Edition Paper on October 5, 2004; DOI 10.1182/blood-2004-06-2188. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-06-2188v1 105/3/1187    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 Dong, C. Articles by Clayberger, C. Search for Related Content PubMed PubMed Citation Articles by Dong, C. Articles by Clayberger, C. Related Collections Immunobiology Apoptosis Cell Cycle Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY A novel apoptosis pathway activated by the carboxyl terminus of p21 Chen Dong, Qing Li, Shu-chen Lyu, Alan M. Krensky, and Carol Clayberger From the Division of Immunology and Transplantation Biology, Department of Pediatrics, Stanford University, Stanford, CA. Delivery of biologically active peptides into cells may help elucidate intracellular signal transduction pathways, identify additional in vivo functions, and develop new therapeutics. Although p21 was first identified as a major regulator of cell cycle progression, it is now clear that p21 subserves multiple functions. The amino terminus of p21 interacts with cyclins and cyclin-dependent kinases, while the carboxyl terminus interacts with proliferating cell nuclear antigen (PCNA), growth arrest and DNA damage–inducible gene 45 (GADD45), calmodulin, SET, and CCAAT/enhancer binding protein- (C/EBP-). A chimeric peptide, p21-IRS, consisting of the carboxyl terminal domain of p21 conjugated to a pentapeptide (RYIRS) rapidly enters lymphoid cells and activates apoptosis. In the present study, we investigate the molecular events involved in p21-activated apoptosis. Comparison of p21-IRS with other known proapoptotic agents demonstrates that p21-IRS activates a novel apoptotic pathway: mitochondria are central to the process, but caspases and a decrease in m are not involved. Targeting the p21 peptide to specific cell populations may allow development of novel therapies to eliminate aberrant cells in human diseases. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. Zhou, L. McPherson, D. Feng, A. Song, C. Dong, S.-C. Lyu, L. Zhou, X. Shi, Y.-T. Ahn, D. Wang, et al. Kruppel-Like Transcription Factor 13 Regulates T Lymphocyte Survival In Vivo J. Immunol., May 1, 2007; 178(9): 5496 - 5504. [Abstract] [Full Text] [PDF] R. Aneja, A. M. Ghaleb, J. Zhou, V. W. Yang, and H. C. Joshi p53 and p21 Determine the Sensitivity of Noscapine-Induced Apoptosis in Colon Cancer Cells Cancer Res., April 15, 2007; 67(8): 3862 - 3870. [Abstract] [Full Text] [PDF] B. Dublet, A. Ruello, M. Pederzoli, E. Hajjar, M. Courbebaisse, S. Canteloup, N. Reuter, and V. Witko-Sarsat Cleavage of p21/WAF1/CIP1 by Proteinase 3 Modulates Differentiation of a Monocytic Cell Line: MOLECULAR ANALYSIS OF THE CLEAVAGE SITE J. Biol. Chem., August 26, 2005; 280(34): 30242 - 30253. [Abstract] [Full Text] [PDF]

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