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Genetics

D-Index
81
Citations
25659
World Ranking
1521
National Ranking
193

Overview

Simon J. Boulton is affiliated with The Francis Crick Institute in the United Kingdom, where their research focuses on molecular biology and genetics related to DNA repair and cancer therapy. Their work spans several main fields including Biochemistry, Genetics and Molecular Biology, and Medicine, with a strong emphasis on subfields such as Molecular Biology, Oncology, Genetics, Physiology, and Aging.

Research topics explored by Simon J. Boulton include:

  • DNA Repair Mechanisms
  • CRISPR and Genetic Engineering
  • PARP inhibition in cancer therapy
  • Telomeres, Telomerase, and Senescence
  • Genetics, Aging, and Longevity in Model Organisms
  • Advanced biosensing and bioanalysis techniques
  • Genomics and Chromatin Dynamics

Simon J. Boulton has been published extensively in scientific journals, with frequent publication venues comprising:

  • bioRxiv (Cold Spring Harbor Laboratory)
  • Molecular Cell
  • Nature Communications
  • Cell Reports
  • Nature

Notable recent papers include:

  • "Polθ inhibitors elicit BRCA-gene synthetic lethality and target PARP inhibitor resistance," 2021, Nature Communications
  • "Defective ALC1 nucleosome remodeling confers PARPi sensitization and synthetic lethality with HRD," 2020, Molecular Cell
  • "Induction of APOBEC3 Exacerbates DNA Replication Stress and Chromosomal Instability in Early Breast and Lung Cancer Evolution," 2021, Cancer Discovery
  • "Targeting the nucleotide salvage factor DNPH1 sensitizes BRCA -deficient cells to PARP inhibitors," 2021, Science
  • "POLQ seals post-replicative ssDNA gaps to maintain genome stability in BRCA-deficient cancer cells," 2022, Molecular Cell

The scientist has collaborated frequently with other researchers in their field. Frequent co-authors include:

  • Graeme Hewitt
  • Ondrej Beláň
  • David Rueda
  • Matthew D. Newton
  • Roopesh Anand

Best Publications

  • Playing the End Game: DNA Double-Strand Break Repair Pathway Choice

    J. Ross Chapman;Martin R.G. Taylor;Simon J. Boulton

  • Double-strand break repair: 53BP1 comes into focus

    Stephanie Panier;Simon J. Boulton

  • Components of the Ku‐dependent non‐homologous end‐joining pathway are involved in telomeric length maintenance and telomeric silencing

    Simon J. Boulton;Stephen P. Jackson

  • Homologous-recombination-deficient tumours are dependent on Polθ-mediated repair

    Raphael Ceccaldi;Jessica C. Liu;Ravindra Amunugama;Ildiko Hajdu

  • RIF1 Is Essential for 53BP1-Dependent Nonhomologous End Joining and Suppression of DNA Double-Strand Break Resection

    J. Ross Chapman;Patricia Barral;Jean-Baptiste Vannier;Valérie Borel

  • Poly(ADP-ribose)-dependent regulation of DNA repair by the chromatin remodeling enzyme ALC1.

    Dragana Ahel;Zuzana Hořejší;Nicola Wiechens;Sophie E. Polo

  • Identification of a Saccharomyces Cerevisiae Ku80 Homologue: Roles in DNA Double Strand Break Rejoining and in Telomeric Maintenance

    Simon J. Boulton;Stephen P. Jackson

  • Saccharomyces cerevisiae Ku70 potentiates illegitimate DNA double-strand break repair and serves as a barrier to error-prone DNA repair pathways.

    S. J. Boulton;S. P. Jackson

  • REV7 counteracts DNA double-strand break resection and affects PARP inhibition

    Guotai Xu;J. Ross Chapman;Inger Brandsma;Jingsong Yuan

  • RTEL1 Dismantles T Loops and Counteracts Telomeric G4-DNA to Maintain Telomere Integrity

    Jean-Baptiste Vannier;Visnja Pavicic-Kaltenbrunner;Mark I.R. Petalcorin;Hao Ding

  • Poly(ADP-ribose)-binding zinc finger motifs in DNA repair/checkpoint proteins

    Ivan Ahel;Dragana Ahel;Takahiro Matsusaka;Allison J. Clark

  • RTEL1 maintains genomic stability by suppressing homologous recombination.

    Louise J. Barber;Jillian L. Youds;Jillian L. Youds;Jordan D. Ward;Michael J. McIlwraith

  • C. elegans ORFeome version 1.1: experimental verification of the genome annotation and resource for proteome-scale protein expression.

    Jérôme Reboul;Philippe Vaglio;Jean François Rual;Jean François Rual;Philippe Lamesch;Philippe Lamesch

  • The C. elegans homolog of the p53 tumor suppressor is required for DNA damage-induced apoptosis

    Björn Schumacher;Kay Hofmann;Simon Boulton;Anton Gartner

  • Mechanisms of Oncogene-Induced Replication Stress: Jigsaw Falling into Place.

    Panagiotis Kotsantis;Eva Petermann;Simon J. Boulton

  • Cellular functions of the BRCA tumour-suppressor proteins

    Simon Boulton

  • BRCA1-associated exclusion of 53BP1 from DNA damage sites underlies temporal control of DNA repair.

    J. Ross Chapman;J. Ross Chapman;Alex J. Sossick;Simon J. Boulton;Stephen P. Jackson

  • Preventing nonhomologous end joining suppresses DNA repair defects of Fanconi anemia.

    Adele Adamo;Spencer J. Collis;Spencer J. Collis;Carrie A. Adelman;Nicola Silva;Nicola Silva

  • Combined Functional Genomic Maps of the C. elegans DNA Damage Response

    Simon J. Boulton;Anton Gartner;Jérôme Reboul;Philippe Vaglio

  • Caenorhabditis elegans HUS-1 is a DNA damage checkpoint protein required for genome stability and EGL-1-mediated apoptosis

    E. R. Hofmann;E. R. Hofmann;S. Milstein;S. Milstein;S. Milstein;S. J. Boulton;M. J. Ye

Frequent Co-Authors

J. Mark Skehel
J. Mark Skehel MRC Laboratory of Molecular Biology
Stephen C. West
Stephen C. West The Francis Crick Institute
Anton Gartner
Anton Gartner University of Dundee
Charles Swanton
Charles Swanton The Francis Crick Institute
Michael Howell
Michael Howell The Francis Crick Institute
Stephen P. Jackson
Stephen P. Jackson University of Cambridge
Paolo Plevani
Paolo Plevani University of Milan
Nicholas M. Luscombe
Nicholas M. Luscombe The Francis Crick Institute
Peter J. Campbell
Peter J. Campbell Wellcome Sanger Institute
Charlotte M. Niemeyer
Charlotte M. Niemeyer University of Freiburg

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