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Valerie Borel

Researcher at Francis Crick Institute

Publications -  19
Citations -  1548

Valerie Borel is an academic researcher from Francis Crick Institute. The author has contributed to research in topics: DNA replication & Homologous recombination. The author has an hindex of 14, co-authored 17 publications receiving 1238 citations. Previous affiliations of Valerie Borel include French Institute of Health and Medical Research & London Research Institute.

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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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MMS19 links cytoplasmic iron-sulfur cluster assembly to DNA metabolism.

TL;DR: Here, it is demonstrated that MMS19 forms a complex with the cytoplasmic Fe-S assembly (CIA) proteins CIAO1, IOP1, and MIP18, which binds to multiple nuclearFe-S proteins involved in DNA metabolism.
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BOD1L Is Required to Suppress Deleterious Resection of Stressed Replication Forks.

TL;DR: This work implicates BOD1L as a critical regulator of genome integrity that restrains nucleolytic degradation of damaged replication forks and identifies it as a component of this fork protection pathway, which safeguards genome stability after replication stress.
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HELQ promotes RAD51 paralogue-dependent repair to avert germ cell loss and tumorigenesis

TL;DR: A critical role is revealed for HELQ in replication-coupled DNA repair, germ cell maintenance and tumour suppression in mammals and it is established that HELQ interacts directly with the RAD51 paralogue complex BCDX2 and functions in parallel to the Fanconi anaemia pathway to promote efficient homologous recombination at damaged replication forks.
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Stabilization of Reversed Replication Forks by Telomerase Drives Telomere Catastrophe

TL;DR: This work establishes that telomerase binding to reversed replication forks inhibits telomere replication, which can be mimicked by preventing replication fork restart through depletion of RECQ1 or PARG.