Author

S. R. Stowell

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

Immunology· 2 Cell Biology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 3 Organism:mouse· 3 Research Focus:cell type annotation· 2 Research Focus:host-pathogen & immune response· 2 Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:development & morphogenesis· 1 Assay:proteomics· 1

Frequent Co-Authors

M. D. Baruffi· 2 shared R. D. Cummings· 2 shared A. E. C. Seixas Azzolini· 1 shared A. E. Gallman· 1 shared A. Soldatenko· 1 shared C. J. Luckey· 1 shared C. R. d. B. Cardoso· 1 shared D. d. S. Lima-Junior· 1 shared

Activity by Year

2020-2021 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 18 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

2 shared papersCell Biology

M. D. Baruffi

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Innate and adaptive immunity to transfused allogenic red blood cells in mice requires MyD88

A. Soldatenko, L. R. Hoyt, L. Xu, S. Calabro, S. M. Lewis, A. E. Gallman, K. E. Hudson, S. R. Stowell, C. J. Luckey, J. C. Zimring, D. Liu, M. Santhanakrishnan, J. E. Hendrickson, S. C. Eisenbarth

This study shows that MyD88, not TRIF, is required for DC activation and alloantibody response to stored syngeneic RBCs in mice.

bioRxiv · Aug 24, 2021 · PreprintImmunology

Endogenous Galectin-3 is Required for Skeletal Muscle Repair

D. G. Cerri, L. C. Rodrigues, V. M. Alves, J. Machado, V. A. F. Bastos, I. d. C. Kettelhut, L. C. Alberici, S. R. Stowell, M. C. R. Costa, R. D. Cummings, M. D. Baruffi

This study shows that endogenous galectin-3 is essential for skeletal muscle repair and myogenic programming in mice.

bioRxiv · Oct 1, 2020Cell Biology

Galectin-1-deficient mice are protected against Trypanosoma cruzi infection through altered neutrophil migration and production of reactive oxygen species and nitric oxide

T. B. Riul, H. Sales-Campos, D. d. S. Lima-Junior, A. E. C. Seixas Azzolini, C. R. d. B. Cardoso, S. R. Stowell, R. D. Cummings, Y. M. L. Valim, M. D. Baruffi

This study shows that Galectin-1 deficiency in mice reduces T. cruzi parasitemia and increases survival by enhancing neutrophil migration and reactive oxygen species/nitric oxide production.

bioRxiv · Sep 11, 2020 · PreprintImmunology