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Alessandro A. Sartori

Researcher at University of Zurich

Publications -  52
Citations -  5007

Alessandro A. Sartori is an academic researcher from University of Zurich. The author has contributed to research in topics: Homologous recombination & DNA repair. The author has an hindex of 27, co-authored 49 publications receiving 4397 citations. Previous affiliations of Alessandro A. Sartori include Academy of Sciences of the Czech Republic & Paul Scherrer Institute.

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Human CtIP promotes DNA end resection

TL;DR: These findings establish evolutionarily conserved roles for CtIP-like proteins in controlling DSB resection, checkpoint signalling and homologous recombination.
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RIF1 Is Essential for 53BP1-Dependent Nonhomologous End Joining and Suppression of DNA Double-Strand Break Resection

TL;DR: Rif1−/− mice are severely compromised for 53BP1-dependent class switch recombination (CSR) and fusion of dysfunctional telomeres and deletion of Rif1 suppresses toxic nonhomologous end joining (NHEJ) induced by PARP inhibition in Brca1-deficient cells.
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CDK targets Sae2 to control DNA-end resection and homologous recombination.

TL;DR: This work establishes that cell-cycle control of DSB resection in Saccharomyces cerevisiae results from the phosphorylation by CDK of an evolutionarily conserved motif in the Sae2 protein, and shows that mutating Ser’267 of Sae 2 to a non-phosphorylatable residue causes phenotypes comparable to those of a sae2Δ null mutant.
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Deficiency of FANCD2-Associated Nuclease KIAA1018/FAN1 Sensitizes Cells to Interstrand Crosslinking Agents

TL;DR: The link of KIAA1018 to the FA pathway is further strengthened by its recruitment to DNA damage through interaction of its UBZ domain with monoubiquitylated FANCD2, and it is proposed to name KIAa1018 FAN CD2-associated nuclease, FAN1.
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Carcinogenic bacterial pathogen Helicobacter pylori triggers DNA double-strand breaks and a DNA damage response in its host cells.

TL;DR: It is concluded that DNA damage followed by potentially imprecise repair is consistent with the carcinogenic properties of H. pylori and with its mutagenic properties in vitro and in vivo and may contribute to the genetic instability and frequent chromosomal aberrations that are a hallmark of gastric cancer.