Author

K. Pinto

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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Pathology· 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 signaling & trafficking· 1 Research Focus:host-pathogen & immune response· 1 Assay:imaging· 1 Assay:proteomics· 1

Frequent Co-Authors

A. Harriot· 2 shared C. Venegas· 2 shared C. Ward· 2 shared G. Shi· 2 shared J. Kallenbach· 2 shared J. Ursitti· 2 shared A. Coleman· 1 shared A. Grosberg· 1 shared

Activity by Year

2023-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 42 mutual co-author links

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2 shared papersPhysiology

A. Harriot

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2 papers

Recent·Most cited

Acute microtubule changes linked to DMD pathology are insufficient to impair contractile function or enhance contraction-induced injury in healthy muscle

C. Venegas, J. Ursitti, J. Kallenbach, K. Pinto, A. Harriot, A. Coleman, G. Shi, C. Ward

This study investigates the impact of microtubule alterations in DMD muscle, finding no impairment in contractile function but some protection against contraction injury with pharmacologic treatment.

bioRxiv · Jun 19, 2024 · PreprintPhysiology

Myofibrillar malformations that arise in mdx muscle fibers are driven by detyrosinated microtubules

A. Harriot, T. Altair-Morris, C. Venegas, J. Kallenbach, K. Pinto, H. Joca, M.-J. Moutin, G. Shi, J. Ursitti, A. Grosberg, C. Ward

This study identifies detyrosinated microtubules as a driver of myofibrillar malformations in dystrophic skeletal muscle fibers, linking increased deTyr-MT levels to structural impairments.

bioRxiv · Mar 27, 2023 · PreprintPathology