Author

Nathan Kopp

Washington University in St. LouisORCID 0000-0002-0858-3242Unclaimed ORCID profile · follow to get notified of new preprints

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Nathan Kopp1 paper

Biology Disciplines

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Animal Behavior & Cognition· 1 Genetics· 1

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Approach:experimental assay· 2 Organism:mouse· 2 Assay:bulk RNA-seq· 1 Research Focus:cell-cell communication· 1 Research Focus:gene regulatory network inference· 1 Research Focus:host-pathogen & immune response· 1

Frequent Co-Authors

Joseph D. DoughertyiD· 2 shared Susan E. MaloneyiD· 2 shared Harrison W. GabeliD· 1 shared Katherine B. McCulloughiD· 1 shared Katherine McCullough· 1 shared Kayla R. NygaardiD· 1 shared Yating LiuiD· 1 shared

Activity by Year

2019-2020 · peak 1/yr

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7 top collaborators · 17 mutual co-author links

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2 shared papersGenetics

Joseph D. DoughertyORCID

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2 papers

Recent·Most cited

GeneticsHuman Molecular GeneticsPeer-reviewedApr 13, 2020

Functions of Gtf2i and Gtf2ird1 in the developing brain: transcription, DNA-binding, and long term behavioral consequences.

Nathan Kopp, Kayla R. Nygaard, Yating Liu…·Joseph D. Dougherty

This study identifies genomic binding sites of Gtf2i and Gtf2ird1 in the developing brain and assesses their combined effects on transcription and behavior in knockout mice.

33 citations

mouseexperimental assay

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Animal Behavior & CognitionbioRxivPreprintFeb 24, 2019

Gtf2i and Gtf2ird1 mutation are not sufficient to reproduce mouse phenotypes caused by the Williams Syndrome critical region

Nathan Kopp, Katherine McCullough, Susan E. Maloney, Joseph D. Dougherty

This study shows that mutations in Gtf2i and Gtf2ird1 alone cannot reproduce the phenotypes of Williams syndrome caused by deletion of the WSCR region.

DOI 10.1101/558544

mousebulk RNA-seq

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