Author

G. S. Pryhuber

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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Cell Biology· 1 Immunology· 1 Physiology· 1

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 3 Approach:experimental assay· 3 Organism:human· 3 Research Focus:differential expression· 2 Research Focus:host-pathogen & immune response· 2 Assay:bulk RNA-seq· 1 Research Focus:cell-cell communication· 1 Research Focus:development & morphogenesis· 1

Frequent Co-Authors

A. M. Dylag· 2 shared A. Grier· 1 shared A. L. Gill· 1 shared A. McDavid· 1 shared A. R. Falsey· 1 shared A. S. Bais· 1 shared B. J. Aronow· 1 shared C. K. Kuo· 1 shared

Activity by Year

2020-2021 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 21 mutual co-author links

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2 shared papersPhysiology

A. M. Dylag

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

iPSC modeling shows uncompensated mitochondrial mediated oxidative stress underlies early heart failure in hypoplastic left heart syndrome

X. Xu, K. Jin, A. S. Bais, W. Zhu, H. Yagi, T. N. Feinstein, P. Nguyen, J. Criscione, X. Liu, G. Beutner, K. B. Karunakaran, P. Adams, C. K. Kuo, D. Kostka, G. S. Pryhuber, , C. W. Lo

This study uses iPSC-derived cardiomyocytes to show that mitochondrial oxidative stress and ER stress underlie early heart failure in HLHS patients.

bioRxiv · May 9, 2021 · PreprintCell Biology

Low Dose Hyperoxia Primes Airways for Fibrosis in Mice after Influenza A Infection

A. M. Dylag, J. Haak, R. Warren, M. Yee, G. S. Pryhuber, M. A. O'Reilly

The paper shows low-dose neonatal hyperoxia increases TSP-1 expression in mice, which primes lungs for fibrosis after influenza A infection, even when lung function appears normal.

bioRxiv · Jun 17, 2020Physiology

Aberrant newborn T cell and microbiota developmental trajectories predict respiratory compromise during infancy

A. Grier, N. Laniewski, A. L. Gill, H. A. Kessler, H. Huyck, J. Holden-Wiltse, S. Bandyopadhyay, J. Carnahan, A. M. Dylag, D. J. Topham, A. R. Falsey, M. T. Caserta, G. S. Pryhuber, S. R. Gill, A. McDavid, K. M. Scheible

The paper identifies that prenatal antibiotics or infection disrupt T cell and microbiota development, increasing respiratory morbidity risk in infants.

bioRxiv · Jun 16, 2020 · PreprintImmunology