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The Intermediate Filament Synemin Regulates Non-Homologous End Joining in an ATM-Dependent Manner

Standard

The Intermediate Filament Synemin Regulates Non-Homologous End Joining in an ATM-Dependent Manner. / Deville, Sara Sofia; Vehlow, Anne; Förster, Sarah; Dickreuter, Ellen; Borgmann, Kerstin; Cordes, Nils.

in: CANCERS, Jahrgang 12, Nr. 7, 28.06.2020.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Deville, SS, Vehlow, A, Förster, S, Dickreuter, E, Borgmann, K & Cordes, N 2020, 'The Intermediate Filament Synemin Regulates Non-Homologous End Joining in an ATM-Dependent Manner', CANCERS, Jg. 12, Nr. 7. https://doi.org/10.3390/cancers12071717

APA

Deville, S. S., Vehlow, A., Förster, S., Dickreuter, E., Borgmann, K., & Cordes, N. (2020). The Intermediate Filament Synemin Regulates Non-Homologous End Joining in an ATM-Dependent Manner. CANCERS, 12(7). https://doi.org/10.3390/cancers12071717

Vancouver

Deville SS, Vehlow A, Förster S, Dickreuter E, Borgmann K, Cordes N. The Intermediate Filament Synemin Regulates Non-Homologous End Joining in an ATM-Dependent Manner. CANCERS. 2020 Jun 28;12(7). https://doi.org/10.3390/cancers12071717

Bibtex

@article{9f816978bd414a55b0d89503dcff3eca,
title = "The Intermediate Filament Synemin Regulates Non-Homologous End Joining in an ATM-Dependent Manner",
abstract = "The treatment resistance of cancer cells is a multifaceted process in which DNA repair emerged as a potential therapeutic target. DNA repair is predominantly conducted by nuclear events; yet, how extra-nuclear cues impact the DNA damage response is largely unknown. Here, using a high-throughput RNAi-based screen in three-dimensionally-grown cell cultures of head and neck squamous cell carcinoma (HNSCC), we identified novel focal adhesion proteins controlling DNA repair, including the intermediate filament protein, synemin. We demonstrate that synemin critically regulates the DNA damage response by non-homologous end joining repair. Mechanistically, synemin forms a protein complex with DNA-PKcs through its C-terminal tail domain for determining DNA repair processes upstream of this enzyme in an ATM-dependent manner. Our study discovers a critical function of the intermediate filament protein, synemin in the DNA damage response, fundamentally supporting the concept of cytoarchitectural elements as co-regulators of nuclear events.",
author = "Deville, {Sara Sofia} and Anne Vehlow and Sarah F{\"o}rster and Ellen Dickreuter and Kerstin Borgmann and Nils Cordes",
year = "2020",
month = jun,
day = "28",
doi = "10.3390/cancers12071717",
language = "English",
volume = "12",
journal = "CANCERS",
issn = "2072-6694",
publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",
number = "7",

}

RIS

TY - JOUR

T1 - The Intermediate Filament Synemin Regulates Non-Homologous End Joining in an ATM-Dependent Manner

AU - Deville, Sara Sofia

AU - Vehlow, Anne

AU - Förster, Sarah

AU - Dickreuter, Ellen

AU - Borgmann, Kerstin

AU - Cordes, Nils

PY - 2020/6/28

Y1 - 2020/6/28

N2 - The treatment resistance of cancer cells is a multifaceted process in which DNA repair emerged as a potential therapeutic target. DNA repair is predominantly conducted by nuclear events; yet, how extra-nuclear cues impact the DNA damage response is largely unknown. Here, using a high-throughput RNAi-based screen in three-dimensionally-grown cell cultures of head and neck squamous cell carcinoma (HNSCC), we identified novel focal adhesion proteins controlling DNA repair, including the intermediate filament protein, synemin. We demonstrate that synemin critically regulates the DNA damage response by non-homologous end joining repair. Mechanistically, synemin forms a protein complex with DNA-PKcs through its C-terminal tail domain for determining DNA repair processes upstream of this enzyme in an ATM-dependent manner. Our study discovers a critical function of the intermediate filament protein, synemin in the DNA damage response, fundamentally supporting the concept of cytoarchitectural elements as co-regulators of nuclear events.

AB - The treatment resistance of cancer cells is a multifaceted process in which DNA repair emerged as a potential therapeutic target. DNA repair is predominantly conducted by nuclear events; yet, how extra-nuclear cues impact the DNA damage response is largely unknown. Here, using a high-throughput RNAi-based screen in three-dimensionally-grown cell cultures of head and neck squamous cell carcinoma (HNSCC), we identified novel focal adhesion proteins controlling DNA repair, including the intermediate filament protein, synemin. We demonstrate that synemin critically regulates the DNA damage response by non-homologous end joining repair. Mechanistically, synemin forms a protein complex with DNA-PKcs through its C-terminal tail domain for determining DNA repair processes upstream of this enzyme in an ATM-dependent manner. Our study discovers a critical function of the intermediate filament protein, synemin in the DNA damage response, fundamentally supporting the concept of cytoarchitectural elements as co-regulators of nuclear events.

U2 - 10.3390/cancers12071717

DO - 10.3390/cancers12071717

M3 - SCORING: Journal article

C2 - 32605308

VL - 12

JO - CANCERS

JF - CANCERS

SN - 2072-6694

IS - 7

ER -