Author

K. Sofiadis

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

Assay:ChIP-seq· 2 Research Focus:chromatin & epigenetic regulation· 2 Approach:experimental assay· 2 Organism:human· 2 Approach:statistical model· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1

Frequent Co-Authors

A. Papantonis· 2 shared Y. Zhu· 2 shared A. Angelopoulou· 1 shared A. Maya-Mendoza· 1 shared A. Mizi· 1 shared A. Polyzos· 1 shared A. Stavropoulou· 1 shared C. Nikolaou· 1 shared

Activity by Year

2020-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 29 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. Papantonis

Mutual co-authors in cluster

Author profile →

2 papers

Recent·Most cited

Senescent cells cluster CTCF on nuclear speckles to sustain their splicing program

S. Palikyras, V. Varamogianni-Mamatsi, Y. Zhu, S. Ramasamy, A. Mizi, I. Liebermann, A. Stavropoulou, I. Papadionysiou, D. Bartsch, Y. Kargapolova, K. Sofiadis, C. Nikolaou, L. Kurian, M. Oudelaar, M. Barbieri, A. Papantonis

This paper identifies senescence-induced CTCF clusters (SICCs) and shows they sustain the senescence splicing program by repurposing nuclear speckle components.

bioRxiv · Jul 16, 2024 · PreprintCell Biology

Genomic instability is an early event driving chromatin reorganization and escape from oncogene-induced senescence

C. Zampetidis, P. Galanos, A. Angelopoulou, Y. Zhu, T. Karamitros, N. Lagopati, R. Mirzazadeh, A. Polyzos, S. Garnerone, E. G. Gusmao, K. Sofiadis, D. E. Pefani, M. Demaria, N. Crosetto, A. Maya-Mendoza, , V. G. Gorgoulis

The paper identifies an early chromosomal inversion that enables escape from oncogene-induced senescence by activating BHLHE40 and promoting malignant transformation.

bioRxiv · Dec 20, 2020Cell Biology