Author

F. Rossignol

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

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Physiology· 1

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Research Focus:cell type annotation· 1 Assay:clinical cohort / trial· 1 Research Focus:differential expression· 1 Approach:experimental assay· 1 Approach:genetic perturbation / CRISPR· 1 Organism:human· 1 Organism:mouse· 1 Assay:proteomics· 1

Frequent Co-Authors

A. Katz· 1 shared A. Padro· 1 shared C. M. Wilczewski· 1 shared C. Turner· 1 shared G. Maxwell· 1 shared J. D. Bailoo· 1 shared J. Kim· 1 shared J. Lee· 1 shared

Activity by Year

2023-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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1 shared paperPhysiology

A. Katz

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1 paper

Recent·Most cited

ATP1A1-linked diseases require a malfunctioning protein product from one allele

K. Spontarelli, V. C. Young, R. Sweazey, A. Padro, J. Lee, T. Bueso, R. M. Hernandez, J. Kim, A. Katz, F. Rossignol, C. Turner, C. M. Wilczewski, G. Maxwell, M. Holmgren, J. D. Bailoo, , P. Artigas

The paper investigates whether haploinsufficiency from protein-null ATP1A1 variants causes disease, finding that Atp1a1+/- mice are phenotypically normal and a human with a null variant shows no disease features.

bioRxiv · Mar 5, 2023Physiology