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Switching Akt: from survival signaling to deadly response
Interfaculty Institute for Biochemistry, University of Tübingen, Germany; BioApplications Enterprises, Winnipeg, MB, Canada.ORCID iD: 0000-0001-9518-1411
Department of Therapeutic Radiology, Yale School of Medicine, New Haven, USA.
Interfaculty Institute for Biochemistry, University of Tübingen, Tübingen, Germany.
Interfaculty Institute for Biochemistry, University of Tübingen, Germany.
2009 (English)In: Bioessays, ISSN 0265-9247, E-ISSN 1521-1878, Vol. 31, no 5, 492-495 p.Article, review/survey (Refereed) Published
Abstract [en]

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.

Place, publisher, year, edition, pages
John Wiley & Sons, 2009. Vol. 31, no 5, 492-495 p.
Keyword [en]
Akt; apoptosis; oncogenes; oxidative stress; senescence
National Category
Biochemistry and Molecular Biology Cell Biology Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy)
Identifiers
URN: urn:nbn:se:liu:diva-86911DOI: 10.1002/bies.200900005ISI: 000265673600002OAI: oai:DiVA.org:liu-86911DiVA: diva2:583117
Available from: 2013-01-07 Created: 2013-01-07 Last updated: 2017-12-06

Open Access in DiVA

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