Joanna R. Morris

This study shows that 7SK-snRNP components HEXIM1 and LARP7 promote replication fork reversal and homologous recombination under transcription and replication stress, independent of BRCA1.

This study investigates how JMJD5 mutations affect replication fork restart and genome stability in cancer and neurodevelopmental disorders.

This paper develops an embryonic zebrafish xenograft model to assess the efficacy of multi-receptor tyrosine kinase inhibitors in rhabdomyosarcoma, identifying VEGF-A as a potential biomarker for Regorafenib response.

This study identifies SUMO4 as a critical regulator of DNA double-strand break repair by promoting SUMO deconjugation through SENP1 and preventing excessive SUMOylation.

This study demonstrates isotropic expansion of the nucleus using expansion microscopy to investigate nanoscale DNA damage response structures.

This study identifies Pin1-promoted SUMOylation of RNF168 as a mechanism to restrict its chromatin accumulation at DNA damage sites, linking it to cellular radioresistance.

The paper identifies RAD52 as the mediator of synthetic-lethal interactions between BRCA1/2, 53BP1 deficiencies, and DNA polymerase theta loss in murine cells.

The paper evaluates twenty-four anti-SUMO monoclonal antibodies for their sensitivity, specificity, and ability to detect different SUMO conjugation states across multiple assays.

This study shows that SAE2 deacetylation during mitosis biases SUMO2 over SUMO1 conjugation, affecting mitotic fidelity through SUMOylation of NuMA.

This study shows that PrimPol creates single-stranded gaps at bulky DNA adducts, which recruit RAD51 for homologous recombination, facilitating DNA repair in mammalian cells.

This paper identifies GSK3β-mediated phosphorylation of IRF1 at T181, which promotes its ubiquitination and degradation, essential for its transcriptional activity and anti-proliferative function.

This study identifies PIN1-mediated BRCA1 isomerisation as a regulator of replication fork protection through enhanced BRCA1-BARD1-RAD51 interaction, distinct from BRCA1's role in homologous recombination.