Pablo Huertas

The paper identifies miRNA-mediated cell-to-cell communication via extracellular vesicles that enhances DNA repair during the radioadaptive response.

This study shows that Cx43 enhances the effectiveness of BRAF/MEKi by reducing DNA repair, leading to increased DNA damage and cellular senescence, and proposes a novel therapeutic approach using sEVs.

This study identifies AEP's role in promoting radioresistance in breast cancer by modulating the ATR pathway and PPP1R10 levels, showing AEP-high/ATR-low as a biomarker for radioresistant patients.

This paper shows dinaciclib increases radiosensitivity in some cancer cell lines by inhibiting CDK12, reducing BRCA1, and promoting p53-dependent senescence.

The paper identifies PCNA as a substrate of BRCA1/BARD1 ubiquitin E3 activity, showing it promotes replication fork stability and continuous DNA synthesis without requiring Homologous Recomberation or Olaparib resistance.

The paper shows EXO1-mediated ssDNA gap expansion is critical for ATR activation and cell viability in BRCA1-deficient cells, revealing a therapeutic target for BRCA1-mutant cancers.

The paper shows that ADAR2-mediated RNA editing of DNA:RNA hybrids is essential for DNA double strand break repair by facilitating DNA end resection.

The paper investigates how CtIP-mediated alternative splicing of PIF1 affects DNA damage response and cell survival to ionizing radiation.

This study identifies a new role for RAD51 paralogs in regulating double strand break repair pathway choice by limiting Ku complex retention, favoring homology-mediated repair over non-homologous end-joining.