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Your search keyword '"Ponstingl, Hannes"' showing total 6 results
Start Over Author "Ponstingl, Hannes" Publisher cold spring harbor laboratory
6 results on '"Ponstingl, Hannes"'

1. Cancer tolerance to chromosomal instability is driven by Stat1 inactivation in vivo

Author

Schubert, Michael, primary, Hong, Christy, additional, Jilderda, Laura J, additional, Requesens-Rueda, Marta, additional, Tijhuis, Andrea E, additional, Simon, Judith E, additional, Bakker, Petra L, additional, Cooper, Jon, additional, Damaskou, Aristi, additional, Wardenaar, Rene, additional, Bakker, Bjorn, additional, Gupta, Sahil, additional, van den Brink, Anouk, additional, Andrade-Ruiz, Lorena, additional, Koster, Mirjam H., additional, Youssef, Sameh A, additional, Luinenburg, Danielle, additional, Strong, Alex, additional, Engleiter, Thomas, additional, Ponstingl, Hannes, additional, de Haan, Gerald, additional, de Bruin, Alain, additional, Rad, Roland, additional, Nijman, Hans W, additional, Medema, Rene H, additional, van Vugt, Marcel, additional, de Bruyn, Marco, additional, Spierings, Diana C.J., additional, Colome-Thatche, Maria, additional, Vassiliou, George, additional, and Foijer, Floris, additional

Published
2021
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3. Genetic associations at regulatory phenotypes improve fine-mapping of causal variants for twelve immune-mediated diseases

Author

Kundu, Kousik, primary, Mann, Alice L., additional, Tardaguila, Manuel, additional, Watt, Stephen, additional, Ponstingl, Hannes, additional, Vasquez, Louella, additional, Morrell, Nicholas W., additional, Stegle, Oliver, additional, Pastinen, Tomi, additional, Sawcer, Stephen J., additional, Anderson, Carl A., additional, Walter, Klaudia, additional, and Soranzo, Nicole, additional

Published
2020
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4. Variation in PU.1 binding and chromatin looping at neutrophil enhancers influences autoimmune disease susceptibility

Author

Watt, Stephen, primary, Vasquez, Louella, additional, Walter, Klaudia, additional, Mann, Alice L., additional, Kundu, Kousik, additional, Chen, Lu, additional, Yan, Ying, additional, Ecker, Simone, additional, Burden, Frances, additional, Farrow, Samantha, additional, Farr, Ben, additional, Iotchkova, Valentina, additional, Elding, Heather, additional, Mead, Daniel, additional, Tardaguila, Manuel, additional, Ponstingl, Hannes, additional, Richardson, David, additional, Datta, Avik, additional, Flicek, Paul, additional, Clarke, Laura, additional, Downes, Kate, additional, Pastinen, Tomi, additional, Fraser, Peter, additional, Frontini, Mattia, additional, Javierre, Biola-Maria, additional, Spivakov, Mikhail, additional, and Soranzo, Nicole, additional

Published
2019
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5. ATM orchestrates the DNA-damage response to counter toxic non-homologous end-joining at broken replication forks

Author

Balmus, Gabriel, primary, Pilger, Domenic, additional, Coates, Julia, additional, Demir, Mukerrem, additional, Sczaniecka-Clift, Matylda, additional, Barros, Ana, additional, Woods, Michael, additional, Fu, Beiyuan, additional, Yang, Fengtang, additional, Chen, Elisabeth, additional, Ostermaier, Matthias, additional, Stankovic, Tatjana, additional, Ponstingl, Hannes, additional, Herzog, Mareike, additional, Yusa, Kosuke, additional, Munoz Martinez, Francisco, additional, Durant, Stephen T., additional, Galanty, Yaron, additional, Beli, Petra, additional, Adams, David J., additional, Bradley, Allan, additional, Metzakopian, Emmanouil, additional, Forment, Josep V., additional, and Jackson, Stephen P., additional

Published
2018
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6. ATM orchestrates the DNA-damage response to counter toxic non-homologous end-joining at broken replication forks

Author

Stephen P. Jackson, Matylda Sczaniecka-Clift, Domenic Pilger, Mukerrem Demir, Michael Woods, Petra Beli, Josep V. Forment, Kosuke Yusa, Stephen T. Durant, Julia Coates, Hannes Ponstingl, Elisabeth Chen, Anna Barros, Matthias Ostermaier, Beiyuan Fu, Gabriel Balmus, Allan Bradley, Fengtang Yang, Francisco Munoz Martinez, Tatjana Stankovic, Mareike Herzog, Emmanouil Metzakopian, David J. Adams, Yaron Galanty, Balmus, Gabriel [0000-0003-2872-4468], Pilger, Domenic [0000-0001-7339-0685], Yang, Fengtang [0000-0002-3573-2354], Chen, Elisabeth [0000-0003-2129-7985], Ponstingl, Hannes [0000-0001-7573-1703], Durant, Stephen T [0000-0003-4209-7499], Galanty, Yaron [0000-0001-7167-9004], Beli, Petra [0000-0001-9507-9820], Forment, Josep V [0000-0002-7797-2583], Jackson, Stephen P [0000-0001-9317-7937], and Apollo - University of Cambridge Repository

Subjects
DNA End-Joining Repair, endocrine system diseases, Ataxia Telangiectasia Mutated Proteins, Piperazines, law.invention, chemistry.chemical_compound, DNA Ligase ATP, Mice, 0302 clinical medicine, law, Mice, Inbred NOD, DNA Breaks, Double-Stranded, lcsh:Science, chemistry.chemical_classification, Mice, Knockout, 0303 health sciences, biology, BRCA1 Protein, Mouse Embryonic Stem Cells, 3. Good health, Non-homologous end joining, 030220 oncology & carcinogenesis, Female, medicine.drug, DNA Replication, DNA damage, Cell Survival, Science, Antineoplastic Agents, Article, Olaparib, 03 medical and health sciences, Cell Line, Tumor, medicine, Animals, Humans, 030304 developmental biology, DNA ligase, Topoisomerase, Neoplasms, Experimental, chemistry, Drug Resistance, Neoplasm, Mutation, biology.protein, Cancer research, Suppressor, Phthalazines, lcsh:Q, Topotecan, CRISPR-Cas Systems, Homologous recombination
Abstract

Mutations in the ATM tumor suppressor gene confer hypersensitivity to DNA-damaging chemotherapeutic agents. To explore genetic resistance mechanisms, we performed genome-wide CRISPR-Cas9 screens in cells treated with the DNA topoisomerase I inhibitor topotecan. Thus, we here establish that inactivating terminal components of the non-homologous end-joining (NHEJ) machinery or of the BRCA1-A complex specifically confer topotecan resistance to ATM-deficient cells. We show that hypersensitivity of ATM-mutant cells to topotecan or the poly-(ADP-ribose) polymerase (PARP) inhibitor olaparib reflects delayed engagement of homologous recombination at DNA-replication-fork associated single-ended double-strand breaks (DSBs), allowing some to be subject to toxic NHEJ. Preventing DSB ligation by NHEJ, or enhancing homologous recombination by BRCA1-A complex disruption, suppresses this toxicity, highlighting a crucial role for ATM in preventing toxic LIG4-mediated chromosome fusions. Notably, suppressor mutations in ATM-mutant backgrounds are different to those in BRCA1-mutant scenarios, suggesting new opportunities for patient stratification and additional therapeutic vulnerabilities for clinical exploitation., Mutations in the ATM tumor suppressor gene confer hypersensitivity to DNA-damaging chemotherapeutic agents. Here, the authors provide evidence that these hypersensitivities reflect a crucial role for ATM at damaged replication forks being to prevent toxic DNA end-joining leading to chromosome fusions and cell death.

Published
2018
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