Author

M. L. Bristol

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

Click to filter author papers

Cancer Biology· 5

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 5 Organism:human· 5 Assay:proteomics· 3 Assay:bulk RNA-seq· 2 Research Focus:cell signaling & trafficking· 2 Research Focus:host-pathogen & immune response· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell type annotation· 1

Frequent Co-Authors

C. D. James· 5 shared I. M. Morgan· 5 shared X. Wang· 5 shared R. Otoa· 3 shared A. Dubey· 2 shared A. Tadimari Prabhakar· 2 shared C. Fontan· 2 shared C. T. Fontan· 2 shared

Activity by Year

2020-2023 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 35 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

5 shared papersCancer Biology

C. D. James

Mutual co-authors in cluster

Author profile →

5 papers

Recent·Most cited

Human Papillomavirus 16 replication converts SAMHD1 into a homologous recombination factor and promotes its recruitment to replicating viral DNA

C. D. James, A. Youssef, A. Tadimari Prabhakar, R. Otoa, A. Witt, R. L. Lewis, M. L. Bristol, X. Wang, K. Zhang, R. Li, I. M. Morgan

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

bioRxiv · Nov 13, 2023Cancer Biology

Direct interaction with the BRD4 carboxyl-terminal motif (CTM) and TopBP1 is required for human papillomavirus 16 E2 association with mitotic chromatin and plasmid segregation function

A. T. Prabhakar, C. D. James, C. Fontan, R. Otoa, X. Wang, M. L. Bristol, R. D. Hill, A. Dubey, S.-Y. Wu, C.-M. Chiang, I. M. Morgan

This study shows that E2 protein interaction with BRD4's CTM and TopBP1 is essential for HPV16's mitotic chromatin association and plasmid segregation, offering therapeutic targets for viral genome targeting.

bioRxiv · May 25, 2023Cancer Biology

Human papillomavirus 16 E2 interaction with TopBP1 is required for E2 and viral genome stability during the viral life cycle.

A. Tadimari Prabhakar, C. D. James, C. Fontan, R. Otoa, X. Wang, M. L. Bristol, R. D. Hill, A. Dubey, I. M. Morgan

This paper shows that HPV16 and HPV11 E2 proteins require interaction with TopBP1 for stability, and disrupting this interaction with CK2 inhibitors like CX4945 promotes viral genome integration and could be a therapeutic strategy.

bioRxiv · Jan 11, 2023Cancer Biology

Human papillomavirus 16 E2 repression of TWIST1 transcription is a potential mediator of HPV16 cancer outcomes

C. T. Fontan, D. Das, M. L. Bristol, C. D. James, X. Wang, H. Lohner, A. Atfi, I. M. Morgan

This paper shows that HPV16 E2 represses TWIST1 transcription, which may explain the better clinical outcomes in HPV16 positive cancers.

bioRxiv · Sep 25, 2020Cancer Biology

Estrogen attenuates the growth of human papillomavirus positive epithelial cells

M. L. Bristol, C. D. James, X. Wang, C. T. Fontan, I. M. Morgan

This paper shows estrogen reduces growth of HPV-positive epithelial cells through two mechanisms, suggesting it could be a therapeutic for HPV+HNSCC.

bioRxiv · Jan 16, 2020Cancer Biology