Author

J. M. McLendon

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

Biology Disciplines

Click to filter author papers

Physiology· 3 Cell Biology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Organism:mouse· 4 Approach:experimental assay· 3 Research Focus:host-pathogen & immune response· 2 Assay:proteomics· 2 Approach:biophysical modeling· 1 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1

Frequent Co-Authors

B. London· 2 shared D. Matasic· 2 shared R. L. Boudreau· 2 shared X. Zhang· 2 shared A. M. Greiner· 1 shared C. Allamargot· 1 shared C. Brenner· 1 shared C. C. Stein· 1 shared

Activity by Year

2020-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 18 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

2 shared papersPhysiology

B. London

Mutual co-authors in cluster

Author profile →

4 papers

Recent·Most cited

A Specialized Centrosome-Proteasome Axis Mediates Proteostasis and Influences Cardiac Stress through Txlnb

J. M. McLendon, X. Zhang, C. C. Stein, L. M. Baehr, S. C. Bodine, R. L. Boudreau

This study identifies Txlnb as a centrosome-adapter protein that mediates proteostasis in cardiomyocytes, linking centrosomes to the ubiquitin-proteasome system and influencing cardiac stress responses.

bioRxiv · Feb 12, 2024Physiology

Knockout of Sorbs2 in Cardiomyocytes Leads to Dilated Cardiomyopathy in Mice

J. M. McLendon, X. Zhang, D. Matasic, M. Kumar, O. M. Koval, I. M. Grumbach, S. Sadayappan, B. London, R. Boudreau

This study shows that deleting Sorbs2 in cardiomyocytes causes dilated cardiomyopathy in mice, with defects in microtubule polymerization and structural proteins, and links Sorbs2 variants to human cardiac diseases.

bioRxiv · Feb 13, 2022 · PreprintPhysiology

Cardiac Specific Overexpression of Transcription Factor EB (TFEB) in Normal Hearts Induces Pathologic Cardiac Hypertrophy and Lethal Cardiomyopathy

H. C. Kenny, E. T. Weatherford, G. V. Collins, C. Allamargot, T. Gesalla, K. Zimmerman, H. Goel, J. M. McLendon, D.-F. Dai, T. Romac, J. Streeter, D. Abhinav, R. O. Pereira, J. Sharafuddin, L.-S. Song, E. D. Abel

This study shows that cardiac-specific overexpression of TFEB leads to pathologic hypertrophy and lethal cardiomyopathy through mitochondrial dysfunction and fibrosis.

bioRxiv · Feb 16, 2021 · PreprintCell Biology

Modulation of the Cardiac Sodium Channel Nav1.5 Peak and Late Currents by NAD+ Precursors

D. Matasic, J.-Y. Yoon, J. M. McLendon, H. Mehdi, M. S. Schmidt, A. M. Greiner, P. Quinones, G. M. Morgan, R. L. Boudreau, K. Irani, C. Brenner, B. London

This study investigates how NAD+ precursors NR and NAM affect NaV1.5 currents and cardiac electrophysiology, finding NR increases peak INa and reduces INa,L while NAM has mixed effects.

bioRxiv · Feb 20, 2020Physiology