Publications by authors named "Tracey E Beyer"
Cells have evolved an elaborate DNA repair network to ensure complete and accurate DNA replication. Defects in these repair machineries can fuel genome instability and drive carcinogenesis while creating vulnerabilities that may be exploited in therapy. Here, we use nascent chromatin capture (NCC) proteomics to characterize the repair of replication-associated DNA double-strand breaks (DSBs) triggered by topoisomerase 1 (TOP1) inhibitors.
View Article and Find Full Text PDFGenotoxic DNA double-strand breaks (DSBs) can be repaired by error-free homologous recombination (HR) or mutagenic non-homologous end-joining. HR supresses tumorigenesis, but is restricted to the S and G2 phases of the cell cycle when a sister chromatid is present. Breast cancer type 1 susceptibility protein (BRCA1) promotes HR by antagonizing the anti-resection factor TP53-binding protein 1(53BP1) (refs.
View Article and Find Full Text PDFArticle Synopsis
- CYR61 is a protein in the CCN family that influences various biological processes, but its role in cancer is still not fully understood, creating controversy in existing literature.
- Research revealed that CYR61 levels were notably higher in an oesophageal cancer cell line, alongside increased integrin α(V)β5 levels, indicating a potential relationship between them.
- The study demonstrated that the expression of CYR61 impacts cancer cell migration by interacting with integrin α(V)β5, suggesting that these proteins work together in facilitating the movement of cancer cells.