Dual Targeting of Akt and mTORC1 Impairs Repair of DNA Double-Strand Breaks and Increases Radiation Sensitivity of Human Tumor Cells.

Inhibition of mammalian target of rapamycin-complex 1 (mTORC1) induces activation of Akt. Because Akt activity mediates the repair of ionizing radiation-induced DNA double-strand breaks (DNA-DSBs) and consequently the radioresistance of solid tumors, we investigated whether dual targeting of mTORC1...

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Bibliographic Details
Published in:PLoS ONE
Main Authors: Marina Holler, Astrid Grottke, Katharina Mueck, Julia Manes, Manfred Jücker, H Peter Rodemann, Mahmoud Toulany
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2016-01-01
Online Access:http://europepmc.org/articles/PMC4854483?pdf=render