Please use this identifier to cite or link to this item: https://doi.org/10.1006/bbrc.2000.2751
Title: Axin-induced apoptosis depends on the extent of its JNK activation and its ability to down-regulate β-catenin levels
Authors: Neo, S.Y.
Zhang, Y.
Yaw, L.P.
Li, P. 
Lin, S.-C. 
Keywords: β-catenin
Apoptosis
Axin
JNK
MEKK1
Issue Date: 27-May-2000
Citation: Neo, S.Y., Zhang, Y., Yaw, L.P., Li, P., Lin, S.-C. (2000-05-27). Axin-induced apoptosis depends on the extent of its JNK activation and its ability to down-regulate β-catenin levels. Biochemical and Biophysical Research Communications 272 (1) : 144-150. ScholarBank@NUS Repository. https://doi.org/10.1006/bbrc.2000.2751
Abstract: Axin is a multidomain protein that coordinates a variety of critical factors in Wnt signaling and JNK activation. In this study, we found that overexpression of Axin leads to apoptosis in several cell lines. A mutant Axin (Axin-ΔMID) that does not contain the MEKK1-interacting domain and is not capable of activating JNK, has less apoptotic effect. Together with the observations that dominant-negative forms of MEKK1 and JNK1 can attenuate Axin-induced apoptosis, we suggest that JNK activation is required for Axin-mediated apoptosis. Wild-type Axin proteins that can lead to destabilization of β-catenin are more effective at causing cell death than those constructs (Axin-ΔGSK/β-cat, Axin-ΔRGS/GSK/β-cat) that are defective in regulation of β-catenin but still fully capable of JNK activation. Furthermore, enhanced β-catenin signaling by coexpression of β-catenin or PP2Cα attenuate cell death. Taken together, we suggest that the ability of Axin to induce apoptosis is determined by its ability to activate JNK and destabilize β-catenin. (C) 2000 Academic Press.
Source Title: Biochemical and Biophysical Research Communications
URI: http://scholarbank.nus.edu.sg/handle/10635/111796
ISSN: 0006291X
DOI: 10.1006/bbrc.2000.2751
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