Author

B. L. Mouery

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

Biology Disciplines

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Cell Biology· 2 Cancer Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:human· 3 Research Focus:cancer & tumor microenvironment· 2 Research Focus:cell signaling & trafficking· 2 Assay:bulk RNA-seq· 1 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:development & morphogenesis· 1 Assay:proteomics· 1

Frequent Co-Authors

J. G. Cook· 3 shared D. Fleifel· 2 shared A. Corno· 1 shared A. M. House· 1 shared A. N. Littlejohn· 1 shared A. T. Saurin· 1 shared A. Walens· 1 shared B. Ma· 1 shared

Activity by Year

2021-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 23 mutual co-author links

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3 shared papersCell Biology

J. G. Cook

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Author profile →

3 papers

Recent·Most cited

APC/C prevents non-canonical order of cyclin/CDK activity to maintain CDK4/6 inhibitor-induced arrest

B. L. Mouery, E. M. Baker, C. A. Mills, L. E. Herring, D. Fleifel, J. G. Cook

This paper shows APC/C activity is essential to maintain CDK4/6 inhibitor-induced arrest by preventing premature S phase entry through degradation of cyclin A.

bioRxiv · Nov 9, 2023 · PreprintCell Biology

Quantitative Profiling of Adaptation to Cyclin E Overproduction

J. C. Limas, A. N. Littlejohn, A. M. House, K. M. Kedziora, B. L. Mouery, B. Ma, D. Fleifel, A. Walens, M. M. Aleman, D. Dominguez, J. G. Cook

This study examines how mammalian cells adapt to chronic cyclin E overproduction, revealing that adaptation involves downregulation of G1-regulated genes and partial resistance to replication stress.

bioRxiv · Jul 26, 2021Cell Biology

CDK4/6 inhibitors induce replication stress to cause long-term cell cycle withdrawal

L. Crozier, R. Foy, B. L. Mouery, R. H. Whitaker, A. Corno, C. Spanos, T. Ly, J. G. Cook, A. T. Saurin

This study shows CDK4/6 inhibitors cause long-term cell cycle withdrawal by inducing replication stress and p53-dependent effects, linking them to genotoxic stress and potential combination therapies.

bioRxiv · Feb 3, 2021Cancer Biology