Author

Ryan M. Baxley

University of MinnesotaORCID 0000-0002-3286-7990Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:human· 3 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Assay:DNA methylation· 1 Research Focus:gene regulatory network inference· 1 Research Focus:variant calling· 1 Assay:whole-genome sequencing· 1

Frequent Co-Authors

Anja‐Katrin BielinskyiD· 3 shared Colette B. RogersiD· 3 shared Eric A. HendricksoniD· 3 shared Liangjun WangiD· 3 shared Wendy Leung· 3 shared Adam J. Harvey· 1 shared Alexandra Sobeck· 1 shared Alistair T. PagnamentaiD· 1 shared

Activity by Year

2021-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 37 mutual co-author links

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3 shared papersMolecular Biology

Anja‐Katrin BielinskyORCID

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3 papers

Recent·Most cited

Cell type specific suppression of hyper-recombination by human RAD18 is linked to PCNA K164 ubiquitination

Colette B. Rogers, Wendy Leung, Ryan M. Baxley, Rachel E. Kram, Liangjun Wang, Joseph P. Buytendorp, Khoi Le, David A. Largaespada, Eric A. Hendrickson, Anja‐Katrin Bielinsky

The paper shows that RAD18 inactivation in HCT116 cells increases recombination and reduces TLS activity, linked to PCNA K164 ubiquitination, but not SUMOylation.

bioRxiv · Sep 3, 2024 · PreprintMolecular Biology

A PCNA-K164R mutation impinges on origin activation and mitotic DNA synthesis

Wendy Leung, Ryan M. Baxley, Emma L. Traband, Ya‐Chu Chang, Colette B. Rogers, Liangjun Wang, Wesley Durrett, Kendall Bromley, Lidia Fiedorowicz, Tanay Thakar, Anika Tella, Alexandra Sobeck, Eric A. Hendrickson, George‐Lucian Moldovan, Naoko Shima, Anja‐Katrin Bielinsky

This study shows that PCNA-K164 ubiquitination is essential for DNA gap filling during S/G2 phases and regulates mitotic DNA synthesis by influencing FANCD2 and MCM2-7 loading.

Cell Reports · Dec 1, 2023Peer-reviewedMolecular Biology

Bi-allelic MCM10 mutations cause telomere shortening with immune dysfunction and cardiomyopathy

Ryan M. Baxley, Wendy Leung, Megan Schmit, Jacob P. Matson, Lulu Yin, Marissa K. Oram, Liangjun Wang, John Taylor, Jack Hedberg, Colette B. Rogers, Adam J. Harvey, Debashree Basu, Jenny C. Taylor, Alistair T. Pagnamenta, Helene Marie-Pierre Dreau, , Anja‐Katrin Bielinsky

This study identifies bi-allelic MCM10 mutations causing telomere shortening, immune dysfunction, and cardiomyopathy by impairing DNA replication and telomerase activity.

Nature Communications · Mar 12, 2021Peer-reviewedMolecular Biology