Author

M. B. Borror

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· 2

Signature Assays, Organisms & Methods

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Organism:C. elegans· 2 Research Focus:cell signaling & trafficking· 2 Research Focus:development & morphogenesis· 2 Research Focus:chromatin & epigenetic regulation· 1 Approach:experimental assay· 1 Approach:genetic perturbation / CRISPR· 1 Research Focus:metabolism & bioenergetics· 1

Frequent Co-Authors

S. L. Rea· 2 shared A. Garrett· 1 shared A. Kar· 1 shared B. Herron· 1 shared B. L. Kennedy· 1 shared J. Russell· 1 shared M. Cain· 1 shared M. Girotti· 1 shared

Activity by Year

2019-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 27 mutual co-author links

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2 shared papersPathology

S. L. Rea

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2 papers

Recent·Most cited

Inhibition of ATR Reverses a Mitochondrial Respiratory Insufficiency

M. B. Borror, M. Girotti, A. Kar, M. Cain, X. Gao, V. MacKay, B. Herron, S. Bhaskaran, S. Becerra, N. Novy, N. Ventura, T. E. Johnson, B. L. Kennedy, S. L. Rea

This study shows that inhibiting ATR in C. elegans reduces the severity of mitochondrial ETC dysfunction by reversing nucleotide imbalances and restoring translation.

Cells · May 24, 2022Peer-reviewedPathology

The PMK-3 (p38) Mitochondrial Retrograde Response Functions in Intestinal Cells to Extend Life via the ESCRT Machinery.

O. Radetskaya, R. K. Lane, T. Friedman, A. Garrett, M. Nguyen, M. B. Borror, J. Russell, S. L. Rea

This study identifies PMK-3 as a key regulator of life extension in C. elegans following mitochondrial ETC disruption, showing its reliance on ESCRT machinery for cellular signaling.

bioRxiv · Oct 22, 2019 · PreprintPathology