Author

McLane M. Montgomery

East Carolina UniversityORCID 0000-0002-8253-6858Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Cancer Biology· 2 Physiology· 2

Signature Assays, Organisms & Methods

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Assay:bulk RNA-seq· 4 Approach:experimental assay· 3 Organism:human· 3 Assay:ATAC-seq· 2 Research Focus:cancer & tumor microenvironment· 2 Research Focus:cell signaling & trafficking· 2 Research Focus:drug response / drug discovery· 2 Organism:mouse· 2

Frequent Co-Authors

Kelsey H. Fisher‐WellmaniD· 4 shared James T. HageniD· 3 shared Raphael Taiwo ArulebaiD· 3 shared Brett R. ChrestiD· 2 shared Charles Edward ChalfantiD· 2 shared David J. FeithiD· 2 shared Joseph M. McClungiD· 2 shared Myles C. Cabot· 2 shared

Activity by Year

2025-2026 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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4 shared papersPhysiology

Kelsey H. Fisher‐WellmanORCID

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Author profile →

4 papers

Recent·Most cited

The MEK inhibitor trametinib incurs mitochondrial injury and induces innate immune responses in the mouse heart

Kelsey H. Fisher‐Wellman, Richard D. Lutze, Logan G. Kirkland, Ju Youn Beak, Mansi Goyal, Raghu Nagalingam, Samantha M. Morrissey, Peyton B. Sandroni, Wei Huang, Julian D. Bailon, Melissa A. Schroder, Lars A. Albrecht, Ethelyn Ofei, Andrew L. Chin, Thomas D. Green, , Brian C. Jensen

This study shows trametinib causes mitochondrial injury and innate immune activation in mouse hearts, leading to cardiomyopathy and heart failure.

Science Advances · Jul 10, 2026Peer-reviewedPhysiology

microRNA-1 Regulates Metabolic Flexibility in Skeletal Muscle via Pyruvate Metabolism

Ahmed Ismaeel, Bailey D. Peck, McLane M. Montgomery, Benjamin I. Burke, Jensen Z. Goh, Gyumin Kang, Abigail Burrows-Franco, Qin Xia, Katarzyna Goljanek‐Whysall, Brian McDonagh, Jared M. McLendon, Pieter Jan Koopmans, Daniel Jacko, Kirill Schaaf, Wilhelm Bloch, , John Joseph McCarthy

This study shows miR-1 regulates metabolic flexibility in skeletal muscle by controlling pyruvate metabolism, with loss of miR-1 causing metabolic inflexibility and reduced endurance.

Molecular Metabolism · Jun 7, 2025Peer-reviewedPhysiology

Acid ceramidase inhibition enhances BCL-2 targeting in venetoclax-resistant acute myeloid leukemia via a cytotoxic integrated stress response

Johnson Ung, Su‐Fern Tan, Jeremy J.P. Shaw, Maansi Taori, Tess M. Deddens, Giovana da Costa Venancio, McLane M. Montgomery, James T. Hagen, Raphael Taiwo Aruleba, Upendarrao Golla, Arati K. Sharma, B. Bishal Paudel, Irene Sung-Ah Lee, Bhavishya U. Ramamoorthy, Kevin A. Janes, , Thomas P. Loughran

This study shows that inhibiting acid ceramidase (AC) enhances venetoclax's effectiveness in venetoclax-resistant AML by inducing a cytotoxic integrated stress response.

bioRxiv · Jun 6, 2025 · PreprintCancer Biology

Acute myeloid leukemia mitochondria hydrolyze ATP to resist chemotherapy

James T. Hagen, McLane M. Montgomery, Raphael Taiwo Aruleba, Brett R. Chrest, Polina M. Krassovskaia, Thomas D. Green, Emely A. Pacheco, Miki Kassai, Tonya N. Zeczycki, Cameron A. Schmidt, Debajit Bhowmick, Su‐Fern Tan, David J. Feith, Charles Edward Chalfant, Thomas P. Loughran, , Kelsey H. Fisher‐Wellman

This study identifies a bioenergetic mechanism in AML cells where mitochondria consume ATP to resist chemotherapy, offering a target for improving treatment.

Science Advances · Apr 9, 2025Peer-reviewedCancer Biology