HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kawasaki, Y. Articles by Takayama, H. Search for Related Content PubMed PubMed Citation Articles by Kawasaki, Y. Articles by Takayama, H. Pubmed/NCBI databases Compound via MeSH Substance via MeSH

Cell Death-Associated Translocation of Plasma Membrane Components Induced by CTL¹

Yukishige Kawasaki^*, Takako Saito^*, Yoshiko Shirota-Someya, Yuko Ikegami, Hajime Komano, Mi-Heon Lee^2,, Christopher J. Froelich^§, Nobukata Shinohara^3, and Hajime Takayama^4,

^* Section for Bioimages, Division of Fundamental Research, Section for Cellular Immunology, Division of Pioneering Research, Project No.12, Project Research Center, Mitsubishi Kasei Institute of Life Sciences, Tokyo, Japan; and ^§ Department of Medicine, Evanston Northwestern Research Institute, Evanston, IL 60201

In the very early stages of target cell apoptosis induced by CTL, we found that fluorescence of labeling probes of the target plasma membrane, such as N-(3-triethylammoniumpropyl)-4-(p-dibutylaminostyryl)pyridinium dibromide (FM1-43), was translocated into intracellular membrane structures including nuclear envelope and mitochondria. This translocation was associated with the execution of CTL-mediated killing, because neither the CTL-target conjugation alone nor the binding of noncytotoxic Th2 clone with target cell was sufficient to provoke the process. Although FM1-43 translocation was observed in perforin-mediated cytotoxicity, examinations with several other dyes failed to detect the evidence for membrane damages that may cause influx of the dye. Moreover, the translocation was also observed in Fas-dependent apoptosis. These data indicate that the translocation precedes the damage of plasma membrane and intracellular organella in the course of apoptotic cell death and may represent the existence of a membrane trafficking that mediates the translocation of plasma membrane components in the early onset of apoptotic cell death.

This article has been cited by other articles:

				H. Lu, Q. Hou, T. Zhao, H. Zhang, Q. Zhang, L. Wu, and Z. Fan Granzyme M Directly Cleaves Inhibitor of Caspase-Activated DNase (CAD) to Unleash CAD Leading to DNA Fragmentation J. Immunol., July 15, 2006; 177(2): 1171 - 1178. [Abstract] [Full Text] [PDF]

				L. Shi, D. Keefe, E. Durand, H. Feng, D. Zhang, and J. Lieberman Granzyme B Binds to Target Cells Mostly by Charge and Must Be Added at the Same Time as Perforin to Trigger Apoptosis J. Immunol., May 1, 2005; 174(9): 5456 - 5461. [Abstract] [Full Text] [PDF]

				H. Rosen, V. Glukhman, T. Feldmann, E. Fridman, and D. Lichtstein Cardiac Steroids Induce Changes in Recycling of the Plasma Membrane in Human NT2 Cells Mol. Biol. Cell, March 1, 2004; 15(3): 1044 - 1054. [Abstract] [Full Text] [PDF]