Claire D. James

This paper shows E2 activates the DNA damage response by displacing CIP2A from TOPBP1, promoting viral replication and cell proliferation through ATM activation and ATR inhibition.

This study investigates the regulation and function of HPV16 circE7 RNA, showing that m6A modification and IRES-like motifs are critical for its formation and translation, impacting viral replication and transformation.

This study shows that Porphyromonas gingivalis internalins promote HNSCC metastasis and drug resistance by interacting with E-cadherin and activating signaling pathways.

This paper shows that HPV16 requires SMARCAL1 to recruit to viral and host replication forks, which is essential for its life cycle and prevents DNA damage and genome integration.

The paper shows that HPV16+ OPC cell lines lose episomal status in monoculture and proposes fibroblast co-culture to maintain episomal viral genomes.

This study identifies novel host factors interacting with HPV16 E2 during differentiation using proximity proteomics, revealing a cooperative E2-TOPBP1-NCL axis critical for viral genome stability.

This study shows fibroblasts support HPV RNA expression and episomal maintenance but reduce EMT-related expression in HPV+ keratinocytes.

This paper develops a fibroblast co-culture model to predict drug responses in HPV+ cancers and shows it better predicts in vivo outcomes than in vitro alone.

This paper shows HPV16 replication converts SAMHD1 into a homologous recombination factor by phosphorylation, enhancing its recruitment to viral DNA and reducing replication.

This study shows that HPV E7 represses miR-203, leading to LASP1 upregulation and promoting proliferation in HPV-positive cervical cancer.

This paper shows that MARCHF8 stabilizes HPV E7 by degrading CUL1 and UBE2L3, preventing E7 degradation in HPV+ HNC cells.

This paper identifies a mitotic E2-TopBP1 complex that inactivates SIRT1, promoting E2 acetylation and stability through p300, which protects against ubiquitination and proteasomal degradation.

This study shows that HPV16 E2 protein interacts with TopBP1 to mediate plasmid segregation and stability during the viral life cycle, and that this interaction is essential for E2 expression and function.

This study shows that the E2-p53 interaction is critical for HPV16 life cycle, with disruption leading to anti-viral effects like reduced proliferation and increased DNA damage.

This paper shows that CK2 phosphorylation of HPV16 E2 on serine 23 promotes interaction with TopBP1, which is critical for plasmid retention and HPV16 immortalization of keratinocytes.

This study shows WRN regulates cell proliferation and HPV16 life cycle in epithelial differentiation by controlling DNA replication and DNA damage.

This study shows that HPV16 E6 and E7 proteins synergistically repress innate immune gene expression in the context of the full HPV16 genome, with neither protein alone sufficient for repression.

This study shows HPV16 E2 regulates host gene expression in keratinocytes, overlaps with genome-wide effects of HPV16, and correlates with clinical outcomes in head and neck cancers.