Author

H. Ponstingl

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Cell Biology· 2 Cancer Biology· 1

Signature Assays, Organisms & Methods

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Organism:human· 3 Research Focus:cancer & tumor microenvironment· 2 Approach:experimental assay· 2 Research Focus:host-pathogen & immune response· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:drug response / drug discovery· 1 Assay:flow cytometry· 1

Frequent Co-Authors

A. Barros· 1 shared A. Bradley· 1 shared A. Damaskou· 1 shared A. de Bruin· 1 shared A. E. Tijhuis· 1 shared A. Pance· 1 shared A. Strong· 1 shared A. van den Brink· 1 shared

Activity by Year

2018-2021 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 18 mutual co-author links

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1 shared paperCell Biology

A. Barros

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

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

M. Schubert, C. Hong, L. J. Jilderda, M. Requesens-Rueda, A. E. Tijhuis, J. E. Simon, P. L. Bakker, J. Cooper, A. Damaskou, R. Wardenaar, B. Bakker, S. Gupta, A. van den Brink, L. Andrade-Ruiz, M. H. Koster, , F. Foijer

The paper identifies Stat1 inactivation as a mechanism by which aneuploid cancers evade immune surveillance in mice and humans.

bioRxiv · Dec 3, 2021 · PreprintCancer Biology

STEM CELL TECHNOLOGY PROVIDES NOVEL TOOLS TO UNDERSTAND HUMAN VARIATION IN Plasmodium falciparum MALARIA

A. Pance, B. Ling, K. Mwikali, M. Koutsourakis, C. Agu, F. Rouhani, H. Ponstingl, R. Montandon, F. Law, J. C. Rayner

The paper uses stem cell technology to study human genetic variation's impact on Plasmodium falciparum malaria by generating erythrocytes from diverse stem cell lines and analyzing parasite invasion.

bioRxiv · Jun 30, 2021 · PreprintCell Biology

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

G. Balmus, D. Pilger, J. Coates, M. Demir, M. Sczaniecka-Clift, A. Barros, M. Woods, B. Fu, F. Yang, E. Chen, M. Ostermaier, T. Stankovic, H. Ponstingl, M. Herzog, K. Yusa, , S. P. P. Jackson

The paper identifies how ATM counteracts toxic non-homologous end-joining at broken replication forks by showing that loss of NHEJ components or BRCA1-A complex confers resistance to DNA-damaging agents in ATM-deficient cells.

bioRxiv · May 24, 2018Cell Biology