Los, Marek ; Maddika, Subbareddy ; Erb, Bettina ; Schulze-Osthoff, Klaus (2009) Switching Akt: from survival signaling to deadly response BioEssays, 31 (5). pp. 492-495. ISSN 0265-9247
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Official URL: http://doi.org/10.1002/bies.200900005
Related URL: http://dx.doi.org/10.1002/bies.200900005
Abstract
Akt, a protein kinase hyperactivated in many tumors, plays a major role in both cell survival and resistance to tumor therapy. A recent study,1 along with other evidences, shows interestingly, that Akt is not a single-function kinase, but may facilitate rather than inhibit cell death under certain conditions. This hitherto undetected function of Akt is accomplished by its ability to increase reactive oxygen species and to suppress antioxidant enzymes. The ability of Akt to down-regulate antioxidant defenses uncovers a novel Achilles' heel, which could be exploited by oxidant therapies in order to selectively eradicate tumor cells that express high levels of Akt activity.
Item Type: | Article |
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Source: | Copyright of this article belongs to John Wiley & Sons, Inc. |
Keywords: | Akt; Apoptosis; Oncogenes; Oxidative Stress; Senescence. |
ID Code: | 118580 |
Deposited On: | 25 May 2021 13:09 |
Last Modified: | 25 May 2021 13:09 |
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