Author

D. Bennin

Memorial University of Newfoundland

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

Cell Biology· 3 Immunology· 3 Bioengineering· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 6 Research Focus:cell type annotation· 5 Organism:zebrafish· 4 Assay:proteomics· 3 Assay:bulk RNA-seq· 2 Research Focus:cell signaling & trafficking· 2 Research Focus:cell-cell communication· 2 Research Focus:differential expression· 2

Frequent Co-Authors

A. Huttenlocher· 6 shared E. E. Rosowski· 2 shared T. J. Schoen· 2 shared A. Ahmed· 1 shared A. Das· 1 shared A. Horn· 1 shared A. N. Peterson· 1 shared A. Peterson· 1 shared

Activity by Year

2019-2026 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 13 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

6 shared papersCell Biology

A. Huttenlocher

Mutual co-authors in cluster

Author profile →

7 papers

Recent·Most cited

EMMPRIN confers metabolic advantage for monocytes and macrophages to promote disease in a model of multiple sclerosis

D. K. Kaushik, A. Das, C. Silva, C. D’Mello, L. G. N. Almeida, S. Patel, D. Bennin, N. Ghasemi, P. Neri, Antoine Dufour, N. J. Bahlis, M. Xue, V. W. Yong

This study shows that EMMPRIN promotes pro-inflammatory metabolism in monocytes/macrophages, worsening multiple sclerosis, and its deletion reduces disease severity.

Journal of Neuroinflammation · Aug 15, 2026Peer-reviewedImmunology

Neutrophil motility is regulated by both cell intrinsic and endothelial cell ARPC1B

A. N. Peterson, D. Bennin, M. Lasarev, J. Chini, D. J. Beebe, A. Huttenlocher

This study shows that ARPC1B in both neutrophils and endothelial cells regulates neutrophil motility, with endothelial ARPC1B being sufficient to drive neutrophil behavior.

bioRxiv · Nov 16, 2023Cell Biology

Confinement by liquid-liquid interface replicates in vivo neutrophil deformations and elicits bleb based migration

J. H. Schrope, A. Horn, K. Lazorchak, C. W. Tinnen, J. J. Stevens, M. Farooqui, J. Li, D. Bennin, T. Robertson, T. D. Juang, A. Ahmed, C. Li, A. Huttenlocher, D. Beebe

This paper introduces a liquid-liquid interface system to model in vivo neutrophil migration, finding that neutrophils use bleb-based force generation to deform barriers under confining pressures.

bioRxiv · Jun 14, 2023 · PreprintBioengineering

PTP1B phosphatase puts a brake on iPSC-derived neutrophil motility and antimicrobial function

M. Giese, D. Bennin, T. J. Schoen, A. Peterson, J. Brand, H. S. Jung, H. Dinh, I. Slukvin, A. Huttenlocher

This study shows that deleting PTP1B phosphatase enhances iPSC-derived neutrophil motility, antimicrobial function, and response to fungal pathogens.

bioRxiv · Jun 5, 2023 · PreprintImmunology

Citrullination regulates wound responses and tissue regeneration in zebrafish

A. Huttenlocher, N. Golenberg, J. Squirrell, D. Bennin, J. RIndy, P. Pistono, K. Eliceiri, M. Shelef, J. Kang

This study shows that Padi2-mediated citrullination is essential for wound response and tissue regeneration in zebrafish by promoting histone modification and cell proliferation in the notochord bead.

bioRxiv · Dec 27, 2019Cell Biology

Cell type specific gene expression profiling reveals a role for the complement component C3A in neutrophil migration to tissue damage

R. A. Houseright, E. E. Rosowski, P. Y. Lam, S. J. Tauzin, O. Mulvaney, C. N. Dewey, D. Bennin, A. Huttenlocher

This study identifies C3A's role in neutrophil migration to tissue damage using TRAP-seq in zebrafish and shows impaired responses in c3a.1-/- larvae.

bioRxiv · Dec 12, 2019Immunology

Imaging invasive fungal growth and inflammation in NADPH oxidase-deficient zebrafish

A. Huttenlocher, T. J. Schoen, E. E. Rosowski, B. P. Knox, D. Bennin, N. P. Keller

The paper uses zebrafish to study how neutrophil ROS affects fungal growth and inflammation during infection with Aspergillus nidulans, finding that ROS limits fungal growth and reduces inflammation in PHOX-deficient hosts.

bioRxiv · Jul 16, 2019 · PreprintCell Biology