Author

M. Herzog

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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Biochemistry· 1 Cancer Biology· 1 Cell Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Organism:bacteria (other)· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1 Approach:genetic perturbation / CRISPR· 1

Frequent Co-Authors

A. Barros· 1 shared A. Bradley· 1 shared A. L. Goldman· 1 shared B. Fu· 1 shared D. J. Adams· 1 shared D. Pilger· 1 shared E. Chen· 1 shared E. Metzakopian· 1 shared

Activity by Year

2018-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 28 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

CO2 Reduction by the Iron Nitrogenase Competes with N2 Fixation Under Physiological Conditions

N. N. Oehlmann, F. V. Schmidt, M. Herzog, A. L. Goldman, J. G. Rebelein

This study shows the Fe nitrogenase in Rhodobacter capsulatus is more efficient at reducing CO2 than Mo nitrogenase but less selective for N2, leading to increased CO2 reduction to methane under physiological conditions.

bioRxiv · Nov 30, 2023Biochemistry

Monitoring plasma nucleosome concentrations to measure of disease response and progression in dogs with hematopoietic malignancies.

H. Wilson-Robles, E. Warry, T. Miller, J. Jarvis, M. Matsushita, P. Miller, M. Herzog, J.-V. Turatsinze, T. K. Kelly, T. K. Butera, G. Michel

This study measures plasma nucleosome concentrations in dogs with hematopoietic malignancies to assess treatment response and disease progression, finding higher concentrations correlate with worse outcomes.

bioRxiv · Feb 2, 2023Cancer 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