Author

R. M. Hernandez

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 F. Rossignol· 1 shared G. Maxwell· 1 shared J. D. Bailoo· 1 shared J. Kim· 1 shared

Activity by Year

2023-2023 · peak 1/yr

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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

PhysiologybioRxivMar 5, 2023

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

K. Spontarelli, V. C. Young, R. Sweazey…·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.

DOI 10.1016/j.bbamcr.2023.119572

mousehuman

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