Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.


Sci. STKE, 12 June 2001
Vol. 2001, Issue 86, p. tw7
[DOI: 10.1126/stke.2001.86.tw7]

EDITORS' CHOICE

Apoptosis Death by Cathepsin B

Apoptosis (programmed cell death) is defined by specific biochemical and morphological markers that include chromatin condensation and fragmentation. Evidence is mounting that pathways involving cathepsins may be important for apoptotic cell death. Foghsgaard et al. show that certain human tumor cell lines can actually be sensitized to apoptosis triggered by activation of tumor necrosis factor receptor 1 (TNFR1) by drugs that inhibit the caspases. Using various methods, cathepsin B was found to be the essential enzyme responsible for this alternative pathway to apoptotic cell death. Furthermore, activation of TNFR1 led specifically to the redistribution of cathepsin B from the lysosome without disrupting the lysosome pH gradient or membrane integrity. This pathway involving cathepsin B was relevant for apoptotic cell death induced by TNFR1 activation and not other stimuli that lead to apoptosis, such as DNA damage, oxidative stress, or heat shock. This pathway was also not particularly important for primary cells or early passage embryo fibroblasts, as opposed to its importance in several human tumor cell lines tested.

L. Foghsgaard, D. Wissing, D. Mauch, U. Lademann, L. Bastholm, M. Boes, F. Elling, M. Leist, M. Jäättelä, Cathepsin B acts as a dominant execution protease in tumor cell apoptosis induced by tumor necrosis factor. J. Cell. Biol. 153, 999-1009 (2001). [Abstract] [Full Text]

Citation: Death by Cathepsin B. Sci. STKE 2001, tw7 (2001).



To Advertise     Find Products


Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882