Label-Free Protein-RNA Interactome Analysis Identifies Khsrp Signaling 
Downstream of the p38/Mk2 Kinase Complex as a Critical Modulator of Cell Cycle 
Progression

Boucas, J.; Fritz, C.; Schmitt, A.; Riabinska, A.; Thelen, L.; Peifer, M.; Leeser, U.; Nuernberg, P.; Altmueller, J.; Gaestel, M.; Dieterich, C.; Reinhardt, H. C.

doi:10.1371/journal.pone.0125745

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Label-Free Protein-RNA Interactome Analysis Identifies Khsrp Signaling Downstream of the p38/Mk2 Kinase Complex as a Critical Modulator of Cell Cycle Progression

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Boucas, J.
Bioinformatics, Core Facilities, Max Planck Institute for Biology of Ageing, Max Planck Society;

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Dieterich, C.
Dieterich – Computational RNA Biology and Ageing, Research Groups, Max Planck Institute for Biology of Ageing, Max Planck Society;

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http://www.ncbi.nlm.nih.gov/pubmed/25993413
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Citation

Boucas, J., Fritz, C., Schmitt, A., Riabinska, A., Thelen, L., Peifer, M., et al. (2015). Label-Free Protein-RNA Interactome Analysis Identifies Khsrp Signaling Downstream of the p38/Mk2 Kinase Complex as a Critical Modulator of Cell Cycle Progression. PLoS One, 10(5), e0125745. doi:10.1371/journal.pone.0125745.

Cite as: https://hdl.handle.net/21.11116/0000-000B-B34A-8

Abstract

Growing evidence suggests a key role for RNA binding proteins (RBPs) in genome stability programs. Additionally, recent developments in RNA sequencing technologies, as well as mass-spectrometry techniques, have greatly expanded our knowledge on protein-RNA interactions. We here use full transcriptome sequencing and label-free LC/MS/MS to identify global changes in protein-RNA interactions in response to etoposide-induced genotoxic stress. We show that RBPs have distinct binding patterns in response to genotoxic stress and that inactivation of the RBP regulator module, p38/MK2, can affect the entire spectrum of protein-RNA interactions that take place in response to stress. In addition to validating the role of known RBPs like Srsf1, Srsf2, Elavl1 in the genotoxic stress response, we add a new collection of RBPs to the DNA damage response. We identify Khsrp as a highly regulated RBP in response to genotoxic stress and further validate its role as a driver of the G(1/)S transition through the suppression of Cdkn1a(P21) transcripts. Finally, we identify KHSRP as an indicator of overall survival, as well as disease free survival in glioblastoma multiforme.