Author

E. P. Hertz

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

Biology Disciplines

Click to filter author papers

Cell Biology· 2

Signature Assays, Organisms & Methods

Click to filter · or open tag

Organism:human· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:chromatin & epigenetic regulation· 1 Assay:DNA methylation· 1 Approach:experimental assay· 1 Approach:genetic perturbation / CRISPR· 1 Assay:proteomics· 1

Frequent Co-Authors

A. Kettenbach· 2 shared J. Duro· 2 shared J. Nilsson· 2 shared B. Lopez Mendez· 1 shared B. Lopez-Mendez· 1 shared B. McEwan· 1 shared B. Rymarczyk· 1 shared G. Montoya· 1 shared

Activity by Year

2021-2021 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 35 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

2 shared papersCell Biology

A. Kettenbach

Mutual co-authors in cluster

Author profile →

2 papers

Recent·Most cited

Cellular toxicity of iHAP1 and DT-061 does not occur through PP2A-B56 targeting

G. Vit, J. Duro, G. Rajendraprasad, E. P. Hertz, L. Holland, M. B. Weisser, B. McEwan, B. Lopez-Mendez, G. Montoya, N. Mailand, K. Maeda, A. Kettenbach, J. Nilsson

This study challenges previous claims that iHAP1 and DT-061 target PP2A-B56 complexes, showing instead that they exert toxicity through microtubule disruption and ER/Golgi disruption, respectively.

bioRxiv · Jul 8, 2021Cell Biology

A complex of BRCA2 and PP2A-B56 is required for DNA repair by homologous recombination

S. M. Ambjoern, J. P. Duxin, E. P. Hertz, I. Nasa, J. Duro, T. Kruse, B. Lopez Mendez, B. Rymarczyk, L. E. Cressey, T. Hansen, A. Kettenbach, V. H. Oestergaard, M. Lisby, J. Nilsson

This study identifies the BRCA2-PP2A-B56 complex as essential for efficient DNA repair by homologous recombination and shows that cancer mutations disrupt this interaction, increasing sensitivity to PARP inhibition.

bioRxiv · Apr 10, 2021Cell Biology