Author

R. Culp-Hill

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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Immunology· 1 Pharmacology & Toxicology· 1 Physiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Research Focus:host-pathogen & immune response· 3 Assay:metabolomics· 3 Organism:human· 2 Assay:ATAC-seq· 1 Research Focus:cell type annotation· 1 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:metabolism & bioenergetics· 1

Frequent Co-Authors

A. D'Alessandro· 3 shared A. Goodspeed· 1 shared A. J. Jezewski· 1 shared A. L. Rachubinski· 1 shared A. R. Odom John· 1 shared B. Kain· 1 shared D. E. Kahn· 1 shared E. Danis· 1 shared

Activity by Year

2019-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 19 mutual co-author links

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3 shared papersImmunology

A. D'Alessandro

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3 papers

Recent·Most cited

Hematopoietic stem cells are a long-term reservoir for trained immunity in a mouse model of chronic autoimmune disease

T. S. Mills, B. Kain, M. T. Burchill, E. Danis, A. Goodspeed, R. Culp-Hill, S. Ferrara, J. R. Roede, A. D'Alessandro, K. Y. King, E. M. Pietras

The paper shows hematopoietic stem cells (HSCs) in a mouse model of chronic autoimmune disease serve as a long-term reservoir for trained immunity, with macrophages derived from them exhibiting increased inflammatory activity and reduced metabolic function.

bioRxiv · May 20, 2022 · PreprintImmunology

Targeting host glycolysis as a strategy for antimalarial development.

A. J. Jezewski, Y.-H. Lin, J. A. Reisz, R. Culp-Hill, Y. Barekatain, V. C. Yan, A. D'Alessandro, F. L. Muller, A. R. Odom John

The paper investigates enolase inhibitors' effects on erythrocytes and their implications for antimalarial therapy by examining red blood cell homeostasis and parasite growth.

bioRxiv · Oct 9, 2020 · PreprintPharmacology & Toxicology

Trisomy 21 activates the kynurenine pathway via increased dosage of interferon receptors

R. K. Powers, K. D. Sullivan, R. Culp-Hill, M. P. Ludwig, K. P. Smith, K. A. Waugh, R. Minter, K. D. Tuttle, H. C. Lewis, A. L. Rachubinski, R. E. Granrath, R. B. Wilkerson, D. E. Kahn, M. Joshi, A. D'Alessandro, , J. M. Espinosa

This study identifies a mechanism by which Trisomy 21 increases kynurenine pathway activity through overexpression of interferon receptors, leading to immunosuppression and neurotoxicity in Down syndrome.

bioRxiv · Jan 11, 2019Physiology