Author

Frederick F. Peelor

Oklahoma Medical Research Foundation

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· 1 Molecular Biology· 1 Physiology· 1

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 3 Organism:mouse· 2 Research Focus:differential expression· 1 Approach:experimental assay· 1 Approach:genetic perturbation / CRISPR· 1 Organism:human· 1 Approach:statistical model· 1

Frequent Co-Authors

Benjamin F. MilleriD· 3 shared Aleksandra Fesiuk· 1 shared Catherine J. King· 1 shared Christiana J. Raymond‐PopeiD· 1 shared Daniel J. Ansel· 1 shared David R. AmiciiD· 1 shared Hae Ryong KwoniD· 1 shared Hem Sapkota· 1 shared

Activity by Year

2024-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 22 mutual co-author links

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3 shared papersPhysiology

Benjamin F. MillerORCID

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Overactive PDGFRα and PDGFRβ promote distinct yet overlapping phenotypes of skeletal muscle fibrosis and stiffness, with PDGFRβ also driving drastic muscle growth

Mariola Gimła, Szczepan S. Olszewski, Jacob L. Brown, Christiana J. Raymond‐Pope, Sandra Rigsby, Frederick F. Peelor, Hae Ryong Kwon, Longbiao Yao, Lorin E. Olson, Jordan D. Fuqua, Benjamin F. Miller

This study shows that overactive PDGFRα and PDGFRβ signaling in mice leads to distinct but overlapping fibrotic and growth-related muscle changes, with sex-specific effects.

bioRxiv · Jan 2, 2026 · PreprintPhysiology

HSF1 remodels mitochondrial biogenesis and function in cancer cells via TIMM17A

Ngoc G.T. Nguyen, Hem Sapkota, Yoko Shibata, Aleksandra Fesiuk, Matthew D. Antalek, Vibhavari Sail, Daniel J. Ansel, David R. Amici, Frederick F. Peelor, Holly Van Remmen, Benjamin F. Miller, Marc L. Mendillo, Richard I. Morimoto, Jian Li

This study identifies TIMM17A as a key mediator of HSF1-driven mitochondrial biogenesis and function in cancer cells, revealing a mechanism linking HSF1 to mitochondrial protein import and energy production.

bioRxiv · May 12, 2025 · PreprintCell Biology

Hyperactive mTORC1/4EBP1 Signaling Dysregulates Proteostasis and Accelerates Cardiac Aging.

Weronika Zarzycka, Kamil Aleksander Kobak, Catherine J. King, Frederick F. Peelor, Benjamin F. Miller, Ying Ann Chiao

This study shows that hyperactive mTORC1/4EBP1 signaling accelerates cardiac aging by dysregulating proteostasis in mice.

GeroScience · Oct 8, 2024Peer-reviewedMolecular Biology