Browsing Cancer Biology by author "Niedzwiedz, Wojciech"
Now showing items 1-9 of 9
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Actin nucleators safeguard replication forks by limiting nascent strand degradation.
Nieminuszczy, J; Martin, PR; Broderick, R; Krwawicz, J; Kanellou, A; et al. (OXFORD UNIV PRESS, 2023-07-07)Accurate genome replication is essential for all life and a key mechanism of disease prevention, underpinned by the ability of cells to respond to replicative stress (RS) and protect replication forks. These responses rely ... -
Active mRNA degradation by EXD2 nuclease elicits recovery of transcription after genotoxic stress.
Sandoz, J; Cigrang, M; Zachayus, A; Catez, P; Donnio, L-M; et al. (NATURE PORTFOLIO, 2023-01-20)The transcriptional response to genotoxic stress involves gene expression arrest, followed by recovery of mRNA synthesis (RRS) after DNA repair. We find that the lack of the EXD2 nuclease impairs RRS and decreases cell ... -
ATR Is a Therapeutic Target in Synovial Sarcoma.
Jones, SE; Fleuren, EDG; Frankum, J; Konde, A; Williamson, CT; et al. (AMER ASSOC CANCER RESEARCH, 2017-12-15)Synovial sarcoma (SS) is an aggressive soft-tissue malignancy characterized by expression of SS18-SSX fusions, where treatment options are limited. To identify therapeutically actionable genetic dependencies in SS, we ... -
Branchpoint translocation by fork remodelers as a general mechanism of R-loop removal.
Hodson, C; van Twest, S; Dylewska, M; O'Rourke, JJ; Tan, W; et al. (CELL PRESS, 2022-12-06)Co-transcriptional R loops arise from stalling of RNA polymerase, leading to the formation of stable DNA:RNA hybrids. Unresolved R loops promote genome instability but are counteracted by helicases and nucleases. Here, we ... -
EXD2 Protects Stressed Replication Forks and Is Required for Cell Viability in the Absence of BRCA1/2.
Nieminuszczy, J; Broderick, R; Bellani, MA; Smethurst, E; Schwab, RA; et al. (CELL PRESS, 2019-08-08)Accurate DNA replication is essential to preserve genomic integrity and prevent chromosomal instability-associated diseases including cancer. Key to this process is the cells' ability to stabilize and restart stalled ... -
Pathway choice in the alternative telomere lengthening in neoplasia is dictated by replication fork processing mediated by EXD2's nuclease activity.
Broderick, R; Cherdyntseva, V; Nieminuszczy, J; Dragona, E; Kyriakaki, M; et al. (NATURE PORTFOLIO, 2023-04-27)Telomerase-independent cancer proliferation via the alternative lengthening of telomeres (ALT) relies upon two distinct, largely uncharacterized, break-induced-replication (BIR) processes. How cancer cells initiate and ... -
TopBP1 interacts with BLM to maintain genome stability but is dispensable for preventing BLM degradation.
Blackford, AN; Nieminuszczy, J; Schwab, RA; Galanty, Y; Jackson, SP; et al. (CELL PRESS, 2015-03-19)The Bloom syndrome helicase BLM and topoisomerase-IIβ-binding protein 1 (TopBP1) are key regulators of genome stability. It was recently proposed that BLM phosphorylation on Ser338 mediates its interaction with TopBP1, to ... -
TOPBP1 recruits TOP2A to ultra-fine anaphase bridges to aid in their resolution.
Broderick, R; Nieminuszczy, J; Blackford, AN; Winczura, A; Niedzwiedz, W (NATURE PUBLISHING GROUP, 2015-03-12)During mitosis, sister chromatids must be faithfully segregated to ensure that daughter cells receive one copy of each chromosome. However, following replication they often remain entangled. Topoisomerase IIα (TOP2A) has ... -
WASp modulates RPA function on single-stranded DNA in response to replication stress and DNA damage.
Han, S-S; Wen, K-K; García-Rubio, ML; Wold, MS; Aguilera, A; et al. (NATURE PORTFOLIO, 2022-06-29)Perturbation in the replication-stress response (RSR) and DNA-damage response (DDR) causes genomic instability. Genomic instability occurs in Wiskott-Aldrich syndrome (WAS), a primary immunodeficiency disorder, yet the ...