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Article

Targeting of AKT1 enhances radiation toxicity of human tumor cells by inhibiting DNA-PKcs-dependent DNA double-strand break repair.

Molecular cancer therapeutics - 1 Jul 2008

Toulany Mahmoud, Kehlbach Rainer, Florczak Urszula, Sak Ali, Wang Shaomeng, Chen Jianyong, Lobrich Markus, Rodemann H Peter

Abstract excerpt

We have already reported that epidermal growth factor receptor/phosphatidylinositol 3-kinase/AKT signaling is an important pathway in regulating radiation sensitivity and DNA double-strand break (DNA-dsb) repair of human tumor cells. In the present study, we investigated the effect of AKT1 on DNA-dependent protein kinase catalytic subunit (DNA-PKcs) activity and DNA-dsb repair in irradiated non-small cell lung...

Read the complete abstract on PubMed

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to DNA Breaks, Double-Stranded

Share to Poly(ADP-ribose) Polymerases

Share to Proto-Oncogene Proteins c-akt

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Source

Identifiers

PMID: 18644989
DOI: 10.1158/1535-7163.MCT-07-2200

Genes

AKT1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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Targeting of AKT1 enhances radiation toxicity of human tumor cells by inhibiting DNA-PKcs-dependent DNA double-strand break repair.PMID 18644989Read ↗

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