Author

G. Marozzi

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

Biochemistry· 1 Cell Biology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Research Focus:chromatin & epigenetic regulation· 2 Approach:experimental assay· 2 Approach:biophysical modeling· 1 Research Focus:cell signaling & trafficking· 1 Assay:cryo-EM· 1 Research Focus:development & morphogenesis· 1 Organism:human· 1 Approach:microscopy & imaging analysis· 1

Frequent Co-Authors

E. Malacaria· 2 shared F. A. Aiello· 2 shared L. Di Biagi· 2 shared M. Honda· 2 shared M. Spies· 2 shared P. Pichierri· 2 shared A. Franchitto· 1 shared A. Stanfield· 1 shared

Activity by Year

2023-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 42 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 papersBiochemistry

E. Malacaria

Mutual co-authors in cluster

Author profile →

2 papers

Recent·Most cited

A double-ring of human RAD52 remodels replication forks restricting fork reversal

M. Honda, M. Razzaghi, P. Gaur, E. Malacaria, G. Marozzi, L. Di Biagi, F. A. Aiello, E. A. Paintsil, A. Stanfield, B. J. Deppe, L. Gakhar, N. J. Schnicker, M. A. Spies, P. Pichierri, M. Spies

The paper shows human RAD52 forms a double-ring structure around stalled replication forks, remodeling them via DNA strand exchange to prevent reversal by SMARCAL1.

bioRxiv · Nov 14, 2023 · PreprintBiochemistry

RAD52 prevents accumulation of Polα-dependent replication gaps at perturbed replication forks

G. Marozzi, L. Di Biagi, E. Malacaria, M. Honda, P. Valenzisi, F. A. Aiello, M. Spies, A. Franchitto, P. Pichierri

This study shows RAD52 prevents Polα-dependent replication gaps by enabling RAD51/Pol repriming at reversed replication forks, which limits DNA damage and improves cell viability during replication stress.

bioRxiv · Apr 12, 2023 · PreprintCell Biology