Publications by authors named "Edgar Pinedo Carpio"
Interstrand DNA cross-links (ICLs) represent complex lesions that compromise genomic stability. Several pathways have been involved in ICL repair, but the extent of factors involved in the resolution of ICL-induced DNA double-strand breaks (DSBs) remains poorly defined. Using CRISPR-based genomics, we identified FIGNL1 interacting regulator of recombination and mitosis (FIRRM) as a sensitizer of the ICL-inducing agent mafosfamide.
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- Homologous recombination (HR) is crucial for repairing DNA double strand breaks and managing replication stress to maintain genome stability and prevent cancer.
- The study focuses on mammalian RAD51 paralogs (RAD51B, RAD51C, RAD51D, XRCC2, and XRCC3), revealing their roles in both DNA repair and the resolution of stalled replication forks, while also uncovering their interaction with RNA metabolic pathways using the BioID approach.
- The findings suggest that these RAD51 paralogs have novel functions in cell biology that could serve as potential biomarkers for breast cancer prognosis, as their RNA expression is linked to poorer patient outcomes.
The heterochromatin protein HP1 plays a central role in the maintenance of genome stability but little is known about how HP1 is controlled. Here, we show that the zinc finger protein POGZ promotes the presence of HP1 at DNA double-strand breaks (DSBs) in human cells. POGZ depletion delays the resolution of DSBs and sensitizes cells to different DNA-damaging agents, including cisplatin and talazoparib.
View Article and Find Full Text PDFSrc family kinases (SFK) are key regulators of cellular proliferation, differentiation, survival, motility and angiogenesis. As such, SFK inhibitors are being tested in clinical trials to prevent metastasis as an alternative to current treatment regimens for a variety of cancers including breast cancer. To contribute to the development of molecular tools improving SFK-targeted therapies, we used the SFK inhibitor dasatinib and a well characterized triple negative breast cancer cell line (BT20).
View Article and Find Full Text PDFIn a genetic screen for regulators of synaptic morphology, we identified the single Caenorhabditis elegans flamingo-like cadherin fmi-1. The fmi-1 mutants exhibit defective axon pathfinding, reduced synapse number, aberrant synapse size and morphology, as well as an abnormal accumulation of synaptic vesicles at nonsynaptic regions. Although FMI-1 is primarily expressed in the nervous system, it is not expressed in the ventral D-type (VD) GABAergic motorneurons, which are defective in fmi-1 mutants.
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