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Angelo Taglialatela
Columbia University
5Publications
3H-index
132Citations
Publications 5
Newest
#1Tarun S. Nambiar (Columbia University)H-Index: 1
#2Pierre Billon (Columbia University)H-Index: 1
Last.Alberto Ciccia (Columbia University)H-Index: 20
view all 13 authors...
Precise editing of genomic DNA can be achieved upon repair of CRISPR-induced DNA double-stranded breaks (DSBs) by homology-directed repair (HDR). However, the efficiency of this process is limited by DSB repair pathways competing with HDR, such as non-homologous end joining (NHEJ). Here we individually express in human cells 204 open reading frames involved in the DNA damage response (DDR) and determine their impact on CRISPR-mediated HDR. From these studies, we identify RAD18 as a stimulator of...
1 CitationsSource
#1Jen-Wei Huang (Columbia University)H-Index: 3
#2Angelo Taglialatela (Columbia University)H-Index: 3
Last.Alberto Ciccia (Columbia University)H-Index: 20
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Homologous recombination (HR) mediates the error-free repair of DNA double-strand breaks to maintain genomic stability. HR is carried out by a complex network of DNA repair factors. Here we identify C17orf53/MCM8IP, an OB-fold containing protein that binds ssDNA, as a novel DNA repair factor involved in HR. MCM8IP-deficient cells exhibit HR defects, especially in long-tract gene conversion, occurring downstream of RAD51 loading, consistent with a role for MCM8IP in HR-dependent DNA synthesis. Mo...
Source
#1David Billing (Columbia University)H-Index: 2
#2Michiko Horiguchi (Columbia University)H-Index: 1
Last.Richard Baer (Columbia University)H-Index: 46
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Summary The BRCA1 tumor suppressor preserves genome integrity through both homology-directed repair (HDR) and stalled fork protection (SFP). In vivo, BRCA1 exists as a heterodimer with the BARD1 tumor suppressor, and both proteins harbor a phosphate-binding BRCT domain. Here, we compare mice with mutations that ablate BRCT phospho-recognition by Bard1 (Bard1S563F and Bard1K607A) or Brca1 (Brca1S1598F). Brca1S1598F abrogates both HDR and SFP, suggesting that both pathways are likely impaired in m...
13 CitationsSource
#1Angelo Taglialatela (CUMC: Columbia University Medical Center)H-Index: 3
#2Silvia Alvarez (CUMC: Columbia University Medical Center)H-Index: 1
Last.Alberto Ciccia (CUMC: Columbia University Medical Center)H-Index: 20
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Summary To ensure the completion of DNA replication and maintenance of genome integrity, DNA repair factors protect stalled replication forks upon replication stress. Previous studies have identified a critical role for the tumor suppressors BRCA1 and BRCA2 in preventing the degradation of nascent DNA by the MRE11 nuclease after replication stress. Here we show that depletion of SMARCAL1, a SNF2-family DNA translocase that remodels stalled forks, restores replication fork stability and reduces t...
67 CitationsSource
#1Marko Vujanovic (UZH: University of Zurich)H-Index: 3
#2Jana Krietsch (UZH: University of Zurich)H-Index: 3
Last.Massimo Lopes (UZH: University of Zurich)H-Index: 34
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Summary DNA damage tolerance during eukaryotic replication is orchestrated by PCNA ubiquitination. While monoubiquitination activates mutagenic translesion synthesis, polyubiquitination activates an error-free pathway, elusive in mammals, enabling damage bypass by template switching. Fork reversal is driven in vitro by multiple enzymes, including the DNA translocase ZRANB3, shown to bind polyubiquitinated PCNA. However, whether this interaction promotes fork remodeling and template switching in ...
51 CitationsSource
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