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- W4300039804 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." @default.
- W4300039804 created "2022-10-03" @default.
- W4300039804 date "1997-10-01" @default.
- W4300039804 modified "2023-09-25" @default.
- W4300039804 title "Papers to Appear in Forthcoming Issues" @default.
- W4300039804 doi "https://doi.org/10.1006/brcg.1997.0963" @default.
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