Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.febslet.2012.11.018
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dc.titleAMPK mediates a pro-survival autophagy downstream of PARP-1 activation in response to DNA alkylating agents
dc.contributor.authorZhou, J.
dc.contributor.authorNg, S.
dc.contributor.authorHuang, Q.
dc.contributor.authorWu, Y.-T.
dc.contributor.authorLi, Z.
dc.contributor.authorYao, S.Q.
dc.contributor.authorShen, H.-M.
dc.date.accessioned2014-06-23T05:31:45Z
dc.date.available2014-06-23T05:31:45Z
dc.date.issued2013-01-16
dc.identifier.citationZhou, J., Ng, S., Huang, Q., Wu, Y.-T., Li, Z., Yao, S.Q., Shen, H.-M. (2013-01-16). AMPK mediates a pro-survival autophagy downstream of PARP-1 activation in response to DNA alkylating agents. FEBS Letters 587 (2) : 170-177. ScholarBank@NUS Repository. https://doi.org/10.1016/j.febslet.2012.11.018
dc.identifier.issn00145793
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/75552
dc.description.abstractIn this study we aim to elucidate the signaling pathway and biological function of autophagy induced by MNNG, a commonly used DNA alkylating agent. We first observed that MNNG is able to induce necrotic cell death and autophagy in Bax-/- Bak-/- double knockout MEFs. We analyzed the critical role of PARP-1 activation and ATP depletion in MNNG-mediated cell death and autophagy via AMPK activation and mTOR suppression. We provide evidence that suppression of AMPK blocks MNNG-induced autophagy and enhances cell death, suggesting the pro-survival function of autophagy in MNNG-treated cells. Taken together, data from this study reveal a novel mechanism in controlling MNNG-mediated autophagy via AMPK activation downstream of PARP-1 activation and ATP depletion. © 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.febslet.2012.11.018
dc.sourceScopus
dc.subjectAlkylating agent
dc.subjectAMPK
dc.subjectAutophagy
dc.subjectDNA damage
dc.subjectNecrosis
dc.subjectPARP-1
dc.typeArticle
dc.contributor.departmentLIFE SCIENCES INSTITUTE
dc.contributor.departmentSAW SWEE HOCK SCHOOL OF PUBLIC HEALTH
dc.contributor.departmentCHEMISTRY
dc.description.doi10.1016/j.febslet.2012.11.018
dc.description.sourcetitleFEBS Letters
dc.description.volume587
dc.description.issue2
dc.description.page170-177
dc.description.codenFEBLA
dc.identifier.isiut000313635400010
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