Please use this identifier to cite or link to this item:
https://doi.org/10.1006/bbrc.2000.2751
DC Field | Value | |
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dc.title | Axin-induced apoptosis depends on the extent of its JNK activation and its ability to down-regulate β-catenin levels | |
dc.contributor.author | Neo, S.Y. | |
dc.contributor.author | Zhang, Y. | |
dc.contributor.author | Yaw, L.P. | |
dc.contributor.author | Li, P. | |
dc.contributor.author | Lin, S.-C. | |
dc.date.accessioned | 2014-11-28T02:49:47Z | |
dc.date.available | 2014-11-28T02:49:47Z | |
dc.date.issued | 2000-05-27 | |
dc.identifier.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 | |
dc.identifier.issn | 0006291X | |
dc.identifier.uri | http://scholarbank.nus.edu.sg/handle/10635/111796 | |
dc.description.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. | |
dc.description.uri | http://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1006/bbrc.2000.2751 | |
dc.source | Scopus | |
dc.subject | β-catenin | |
dc.subject | Apoptosis | |
dc.subject | Axin | |
dc.subject | JNK | |
dc.subject | MEKK1 | |
dc.type | Article | |
dc.contributor.department | INSTITUTE OF MOLECULAR & CELL BIOLOGY | |
dc.description.doi | 10.1006/bbrc.2000.2751 | |
dc.description.sourcetitle | Biochemical and Biophysical Research Communications | |
dc.description.volume | 272 | |
dc.description.issue | 1 | |
dc.description.page | 144-150 | |
dc.description.coden | BBRCA | |
dc.identifier.isiut | 000087378900025 | |
Appears in Collections: | Staff Publications |
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