Author

Shannon K. Harkins

Michigan State UniversityORCID 0000-0002-7272-9197Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Developmental Biology· 1 Genetics· 1 Physiology· 1

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Approach:experimental assay· 2 Organism:mouse· 2 Research Focus:cell-cell communication· 1 Assay:ChIP-seq· 1 Research Focus:gene regulatory network inference· 1 Organism:human· 1

Frequent Co-Authors

Ronald L. ChandleriD· 3 shared Abigail Z. BennettiD· 2 shared Amelia R. Arendt· 2 shared Hilary J. SkalskiiD· 2 shared Marie AdamsiD· 2 shared Amanda G. Lopez Espinosa· 1 shared Asgerally T. FazleabasiD· 1 shared Brooke Armistead· 1 shared

Activity by Year

2022-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 30 mutual co-author links

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3 shared papersPhysiology

Ronald L. ChandlerORCID

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3 papers

Recent·Most cited

Endometrial Hyperplasia Risk Is Increased by High-Fat Diet Via Estrogen-Driven Stromal Fibroblast Reprogramming Toward a Pro-Fibrotic State

Hilary J. Skalski, Abigail Z. Bennett, Lauren E. Wood, Shannon K. Harkins, Amelia R. Arendt, Amanda G. Lopez Espinosa, Gregory W. Burns, Emmanuel N. Paul, Galen H. Hostetter, Katelyn Becker, Marc Wegener, Marie Adams, Jose M. Teixeira, Kin H. Lau, Ronald L. Chandler

This paper shows that a high-fat diet increases endometrial hyperplasia risk by reprogramming stromal fibroblasts to a pro-fibrotic state driven by estrogen.

bioRxiv · Mar 24, 2026 · PreprintPhysiology

Generation and characterization of a mouse model of conditional Chd4 knockout in the endometrial epithelium.

Shannon K. Harkins, Hilary J. Skalski, Abigail Z. Bennett, Laura A. Pavliscak, Nakati C. Sany, Amelia R. Arendt, Lauren Wood, Genna E. Moldovan, Ronald L. Chandler

This study generates a mouse model with conditional Chd4 knockout in the endometrial epithelium and finds no significant structural or functional changes or tumorigenesis.

PLoS ONE · Dec 19, 2025Peer-reviewedDevelopmental Biology

ARID1A maintains transcriptionally repressive H3.3 associated with CHD4-ZMYND8 chromatin interactions

Jake J. Reske, Mike R. Wilson, Brooke Armistead, Shannon K. Harkins, Cristina Perez, Joel A. Hrit, Marie Adams, Scott B. Rothbart, Stacey A. Missmer, Asgerally T. Fazleabas, Ronald L. Chandler

This study shows ARID1A maintains repressive H3.3 chromatin through interactions with CHD4 and ZMYND8, suppressing genes involved in cell motility and epithelial-to-mesenchymal transition in endometriotic cells.

BMC Biology · Sep 24, 2022Peer-reviewedGenetics