A5054884660- DNA Repair Mechanisms
- PARP inhibition in cancer therapy
- CRISPR and Genetic Engineering
- Ubiquitin and proteasome pathways
- Genomics and Chromatin Dynamics
- Genetic Neurodegenerative Diseases
- PI3K/AKT/mTOR signaling in cancer
- Genetics and Neurodevelopmental Disorders
- Metabolism, Diabetes, and Cancer
- Cancer, Lipids, and Metabolism
- Cancer, Hypoxia, and Metabolism
- Protein Kinase Regulation and GTPase Signaling
- DNA and Nucleic Acid Chemistry
- Cancer-related Molecular Pathways
- Cancer Treatment and Pharmacology
Institute of Cancer Research
2021-2022
University of Birmingham
2016-2019
NIHR Birmingham Biomedical Research Centre
2019
Genomics (United Kingdom)
2019
Centro Nacional de Biotecnología
2014
SUMOylation (small ubiquitin-like modifier) in the DNA double-strand break (DSB) response regulates recruitment, activity, and clearance of repair factors. However, our understanding a role for deSUMOylation this process is limited. Here we identify different mechanistic roles homologous recombination (HR) nonhomologous end joining (NHEJ) through investigation deSUMOylase SENP2. We found that regulated MDC1 prevents excessive its RNF4-VCP mediated from DSBs, thereby promoting NHEJ. In...
Abstract Accurate chromosomal DNA replication is essential to maintain genomic stability. Genetic evidence suggests that certain repetitive sequences impair replication, yet the underlying mechanism poorly defined. Replication could be directly inhibited by template or indirectly, for example DNA-bound proteins. Here, we reconstitute of mono-, di- and trinucleotide repeats in vitro using eukaryotic replisomes assembled from purified We find structure-prone are sufficient replication. Whilst...
// Pedro Torres-Ayuso 1 , Manuel Daza-Martín Jorge Martín-Pérez 2 Antonia Ávila-Flores and Isabel Mérida Department of Immunology Oncology, Centro Nacional de Biotecnología/CSIC, Madrid, Spain Cancer Biology, Instituto Investigaciones Biomédicas Alberto Sols/CSIC, Universidad Autónoma Correspondence: Ávila-Flores, email: Mérida, Keywords : Diacylglycerol kinase, Src, 3D tumor growth, chemotherapy resistance, PI3K/Akt...
The breast cancer type-1 susceptibility protein (BRCA1) contributes to genome integrity through homologous recombinational DNA repair and by protecting stalled replication forks from nucleolytic degradation. We recently discovered that fork protection requires a conformational change of BRCA1 unimportant recombination repair, indicating separate roles for in these pathways.
Abstract BRCA1, BRCA2 and a subset of Fanconi’s Anaemia proteins act to promote RAD51-mediated protection newly synthesised DNA at stalled replication forks from degradation by nucleases. How BRCA1 contributes, how it is regulated whether fork relates to, or differs from, the roles has in homologous recombination not clear. Here we show that canonical BRCA1-PALB2 interaction required for instead demonstrate ability protect nascent an unexpected fashion through conformational change mediated...
Abstract SUMOylation in the DNA double-strand break (DSB) response regulates recruitment, activity and clearance of repair factors. However, our understanding a role for deSUMOylation this process is limited. Here we identify different mechanistic roles homologous recombination (HR) non-homologous enjoining (NHEJ) through investigation deSUMOylase SENP2. We find regulated MDC1 prevents excessive its RNF4-VCP mediated from DSBs, thereby promoting NHEJ. In contrast show HR differentially...
SUMMARY Accurate chromosomal DNA replication is essential to maintain genomic stability. Genetic evidence suggests that certain repetitive sequences impair replication, yet the underlying mechanism poorly defined. Replication could be directly inhibited by template or indirectly, for example DNA-bound proteins. Here, we reconstituted of mono-, di- and trinucleotide repeats in vitro using eukaryotic replisomes assembled from purified We found structure-prone are sufficient replication. Whilst...