Author

N. Salama

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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Cancer Biology· 1 Immunology· 1 Microbiology· 1

Signature Assays, Organisms & Methods

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

Frequent Co-Authors

A. Hartman· 1 shared A. Koehne· 1 shared A. Rodriguez· 1 shared B. P. Bratton· 1 shared C. Gardner· 1 shared C. Leverich· 1 shared C. McMillen· 1 shared D. Boyles· 1 shared

Activity by Year

2020-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 16 mutual co-author links

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1 shared paperImmunology

A. Hartman

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Distinct regions of H. pylori's bactofilin regulate protein interactions to control cell shape

S. R. Sichel, B. P. Bratton, N. Salama

This study identifies regions of H. pylori's bactofilin CcmA that regulate protein interactions and cell shape by controlling polymerization and interactions with Csd5 and Csd7.

bioRxiv · Apr 5, 2022Microbiology

Long-term persistence of viral RNA and inflammation in the CNS of macaques exposed to aerosolized Venezuelan equine encephalitis virus.

H. Ma, J. Albe, T. Gilliland, C. McMillen, C. Gardner, D. Boyles, E. Cottle, M. Dunn, J. Lundy, N. Salama, K. O'Malley, I. Pandrea, T. Teichert, S. Barrick, W. Klimstra, , D. S. Reed

This study shows that VEEV persists in the CNS of macaques long after acute infection, with ongoing inflammation and immune cell infiltration.

bioRxiv · Sep 9, 2021Immunology

Helicobacter pylori accelerates KRAS-dependent gastric dysplasia

V. P. O'Brien, A. Koehne, J. Dubrulle, A. Rodriguez, C. Leverich, P. Kong, J. Campbell, R. Pierce, J. Goldenring, E. Choi, N. Salama

This study shows that Helicobacter pylori infection accelerates KRAS-driven gastric dysplasia in mice by promoting inflammation, altering gene expression, and increasing proliferation of preneoplastic glands.

bioRxiv · Oct 6, 2020Cancer Biology