MassIVE MSV000080795

Imported Reanalysis Dataset Public PXD002135

ATR inhibition rewires cellular signaling networks in response to pathologic replication stress

Description

DNA replication stress is the major cause of genomic instability in human cells. The ataxia telangiectasia and Rad3-related kinase (ATR) plays an essential role in the cellular response to replication stress and inhibition of ATR has emerged as therapeutic strategy for the treatment of cancer. However, the ATR-dependent signaling in the cellular response to replication stress has not been systematically investigated. Here, we employ quantitative mass spectrometry-based proteomics to decipher the ATR-dependent phosphorylation events in response to pathological replication stress induced by hydroxyurea. Our data define the substrate spectrum of ATR and identify several novel putative ATR substrates. In addition, we demonstrate that ATR-inhibition fundamentally rewires cellular signaling networks leading to the prominent activation of different pathways including the ATM-driven double strand break repair. [dataset license: CC0 1.0 Universal (CC0 1.0)]

Keywords: Phosphorytion ; ATR ; Phosphoproteomics

Contact

Principal Investigators:
(in alphabetical order)
Petra Beli, Institute of Molecular Biology (IMB), Mainz, Germany, N/A
Submitting User: ccms

Publications

Wagner SA, Oehler H, Voigt A, Dalic D, Freiwald A, Serve H, Beli P.
ATR inhibition rewires cellular signaling networks induced by replication stress.
Proteomics. 2016 Feb;16(3):402-16.

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Distinct protein accessions are counted across all files submitted in the "Statistical Analysis of Quantified Analytes" category having a "Protein" column in this dataset.

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