Author

A. Piro

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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Bioengineering· 1 Immunology· 1 Microbiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Research Focus:host-pathogen & immune response· 2 Organism:mouse· 2 Research Focus:cell signaling & trafficking· 1 Organism:human· 1

Frequent Co-Authors

J. Coers· 2 shared R. Finethy· 2 shared S. Luoma· 2 shared A. Au· 1 shared A. Haldar· 1 shared A. Yirga· 1 shared C. Lesser· 1 shared C. M. Yip· 1 shared

Activity by Year

2017-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 25 mutual co-author links

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2 shared papersImmunology

J. Coers

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3 papers

Recent·Most cited

Islet-on-a-chip device reveals first phase glucose-stimulated respiration is substrate limited by glycolysis independent of Ca2+ activity.

R. Regeenes, Y. Wang, A. Piro, A. Au, C. M. Yip, M. B. Wheeler, J. V. Rocheleau

The paper develops an islet-on-a-chip device to measure glucose-stimulated respiration and Ca2+ activity in individual islets, showing OxPhos is substrate-limited by NADH rather than ADP and independent of Ca2+.

bioRxiv · Mar 2, 2022Bioengineering

Dynamin-related Irgm proteins modulate LPS-induced caspase-4 activation and septic shock

R. Finethy, J. Dockterman, M. Kutsch, N. Orench-Rivera, G. Wallace, A. Piro, S. Luoma, A. Haldar, S. Hwang, J. Martinez, M. Kuehn, G. Taylor, J. Coers

This study identifies Irgm proteins as negative regulators of caspase-4 activation in response to LPS, showing their role in preventing septic shock.

bioRxiv · Mar 18, 2020Immunology

Detection of cytosolic Shigella flexneri via a C-terminal triple-arginine motif of GBP1 inhibits actin-based motility

A. Piro, D. Hernandez, S. Luoma, E. Feeley, R. Finethy, A. Yirga, E. Frickel, C. Lesser, J. Coers

This paper shows human GBP1 uniquely captures cytosolic Gram-negative bacteria via a C-terminal triple-arginine motif, inhibiting their actin-based motility and cell-to-cell spread, while Shigella uses IpaH9.8 to resist GBP1 targeting.

bioRxiv · Nov 1, 2017Microbiology