Molly L. Bristol

E2 displacement of CIP2A from TOPBP1 activates the DNA damage response during papillomavirus life cycles

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.

HPV16 recruitment of SMARCAL1 to viral and host replication forks is required for the viral life cycle

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 Utility of Fibroblast Co-culture for the Maintenance of Episomes in Human Papillomavirus-Associated Cancer Models

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

Differentiation-Dependent Proximity Proteomics Identifies Novel Host Factors Linked to HPV16 E2 Function

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.

Fibroblasts Regulate the Transformation Potential of Human Papillomavirus-positive Keratinocytes

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

Fibroblast Stromal Support Model for Predicting Human Papillomavirus-Associated Cancer Drug Responses.

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.

A human papillomavirus 16 E2-TopBP1 dependent SIRT1-p300 acetylation switch regulates mitotic viral and human protein levels

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.

Interaction with TopBP1 mediates human papillomavirus 16 E2 plasmid segregation/retention function and stability during the viral life cycle

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.

A critical role for E2-p53 interaction during the human papillomavirus 16 life cycle

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.

CK2 phosphorylation of human papillomavirus 16 E2 on serine 23 promotes interaction with TopBP1 and is critical for E2 plasmid retention function

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.

Human papillomavirus 16 E6 and E7 synergistically repress innate immune gene transcription

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.

Human papillomavirus 16 E2 regulates keratinocyte gene expression relevant to cancer and the viral life cycle

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.