A5054117046- DNA Repair Mechanisms
- CRISPR and Genetic Engineering
- Bacterial Genetics and Biotechnology
- DNA and Nucleic Acid Chemistry
- Genomics and Chromatin Dynamics
- Carcinogens and Genotoxicity Assessment
- RNA and protein synthesis mechanisms
- PARP inhibition in cancer therapy
- Photosynthetic Processes and Mechanisms
- Microtubule and mitosis dynamics
- Plant Genetic and Mutation Studies
- Mitochondrial Function and Pathology
- BRCA gene mutations in cancer
- Advanced biosensing and bioanalysis techniques
- Bacteriophages and microbial interactions
- Cancer therapeutics and mechanisms
- RNA Interference and Gene Delivery
- Chromosomal and Genetic Variations
- Fungal and yeast genetics research
- Telomeres, Telomerase, and Senescence
- Molecular Biology Techniques and Applications
- RNA Research and Splicing
- Plant nutrient uptake and metabolism
- Genetic factors in colorectal cancer
- Advanced Electron Microscopy Techniques and Applications
The Francis Crick Institute
2015-2024
Cancer Research UK
2007-2017
University of Toronto
2017
MRC London Institute of Medical Sciences
2013
University of Oxford
2000-2009
Queen's Medical Centre
1991-2007
University of Virginia
1999-2005
University of Warwick
2005
The Honourable Society of Lincoln's Inn
1993-2003
Massachusetts General Hospital
2003
Posttranslational modifications play key roles in regulating chromatin plasticity. Although various chromatin-remodeling enzymes have been described that respond to specific histone modifications, little is known about the role of poly[adenosine 5'-diphosphate (ADP)-ribose] remodeling. Here, we identify a enzyme, ALC1 (Amplified Liver Cancer 1, also as CHD1L), interacts with poly(ADP-ribose) and catalyzes PARP1-stimulated nucleosome sliding. Our results define DNA damage-response protein...
Bloom's syndrome (BS) is an autosomal recessive disorder associated with dwarfism, immunodeficiency, reduced fertility, and elevated levels of many types cancer. BS cells show marked genomic instability; in particular, hyperrecombination between sister chromatids homologous chromosomes. This instability thought to result from defective processing DNA replication intermediates. The gene mutated BS, BLM , encodes a member the RecQ family DExH box helicases, which also includes Werner's...
POLQ is a key effector of DSB repair by microhomology-mediated end-joining (MMEJ) and overexpressed in many cancers. inhibitors confer synthetic lethality HR Shieldin-deficient cancer cells, which has been proposed to reflect critical dependence on the pathway MMEJ. Whether also operates independent MMEJ remains unexplored. Here, we show that POLQ-deficient cells accumulate post-replicative ssDNA gaps upon BRCA1/2 loss or PARP inhibitor treatment. Biochemically, cooperation between helicase...