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Petr Cejka

Researcher at University of Lugano

Publications -  98
Citations -  6647

Petr Cejka is an academic researcher from University of Lugano. The author has contributed to research in topics: Homologous recombination & DNA repair. The author has an hindex of 38, co-authored 89 publications receiving 5405 citations. Previous affiliations of Petr Cejka include École Polytechnique Fédérale de Lausanne & ETH Zurich.

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DNA end resection by Dna2-Sgs1-RPA and its stimulation by Top3-Rmi1 and Mre11-Rad50-Xrs2

TL;DR: It is established that Dna2, Sgs1 and RPA constitute a minimal protein complex capable of DNA resection in vitro and that both the topoisomerase 3 and Rmi1 complex and the Mre11–Rad50–Xrs2 complex (MRX) have important roles as stimulatory components.
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Pif1 family helicases suppress genome instability at G-quadruplex motifs

TL;DR: It is shown that exceptionally potent G- quadruplex unwinding is conserved among Pif1 helicases, and when expressed in yeast, human PIF1 suppressed both G-quadruplex-associated DNA damage and telomere lengthening.
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Sae2 promotes dsDNA endonuclease activity within Mre11–Rad50–Xrs2 to resect DNA breaks

TL;DR: Using purified Saccharomyces cerevisiae proteins, it is shown that Sae2 promotes ds DNA-specific endonuclease activity by the Mre11 subunit within the MRX complex, demonstrating a probable mechanism for the initiation of dsDNA break processing in both vegetative and meiotic cells.
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DNA2 drives processing and restart of reversed replication forks in human cells

TL;DR: Following prolonged genotoxic stress, DNA2 and WRN functionally interact to degrade reversed replication forks and promote replication restart, thereby preventing aberrant processing of unresolved replication intermediates.
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Restoration of Replication Fork Stability in BRCA1- and BRCA2-Deficient Cells by Inactivation of SNF2-Family Fork Remodelers.

TL;DR: In this paper, the authors show that depletion of SMARCAL1, a SNF2-family DNA translocase that remodels stalled forks, restores replication fork stability and reduces the formation of replication stress-induced DNA breaks and chromosomal aberrations in BRCA1/2-deficient cells.