Author

David B. Everman

Greenwood Genetic CenterORCID 0000-0001-8331-992XUnclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Genetic & Genomic Medicine· 1 Molecular Biology· 1 Neuroscience· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Research Focus:gene regulatory network inference· 1 Organism:human· 1 Organism:mouse· 1 Assay:protein structure· 1

Frequent Co-Authors

Heather R. Flanagan‐SteetiD· 2 shared Acadia M Thielking· 1 shared Adam J. HarringtoniD· 1 shared Ahlem AssaliiD· 1 shared Benjamin M. SiemseniD· 1 shared Brittany T. Truong· 1 shared Catherine BridgesiD· 1 shared Charles E. SchwartziD· 1 shared

Activity by Year

2019-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 21 mutual co-author links

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2 shared papersGenetic & Genomic Medicine

Heather R. Flanagan‐SteetORCID

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Author profile →

3 papers

Recent·Most cited

PRDM1 DNA-binding zinc finger domain is required for normal limb development and is disrupted in Split Hand/Foot Malformation

Brittany T. Truong, Lomeli Carpio Shull, Ezra S. Lencer, Eric G. Bend, Michael J. Field, Elizabeth Blue, Michael J. Bamshad, Cindy D. Skinner, David B. Everman, Charles E. Schwartz, Heather R. Flanagan‐Steet, Kristin Artinger

The paper identifies PRDM1 variants causing Split Hand/Foot Malformation and shows their functional impact on limb development through zebrafish experiments and gene expression analysis.

Disease Models & Mechanisms · Apr 1, 2023Peer-reviewedGenetic & Genomic Medicine

Structural model of PORCN illuminates disease-associated variants and drug binding sites

Jia Yu, Pei-Ju Liao, Weijun Xu, Julie R. Jones, David B. Everman, Heather R. Flanagan‐Steet, Thomas H. Keller, David M. Virshup

The paper develops a structural model of PORCN, revealing its catalytic mechanism, disease-associated variants, and drug binding sites.

Journal of Cell Science · Nov 24, 2021Peer-reviewedMolecular Biology

MEF2C hypofunction in neuronal and neuroimmune populations cooperate to produce MEF2C haploinsufficiency syndrome-like behaviors in mice

Adam J. Harrington, Catherine Bridges, Kayla Blankenship, Ahlem Assali, Stefano Berto, Benjamin M. Siemsen, Hannah Warren Moore, Jennifer Y. Cho, Evgeny Tsvetkov, Acadia M Thielking, Geneviève Konopka, David B. Everman, Michael D. Scofield, Steven A. Skinner, Christopher W. Cowan

This study shows that MEF2C hypofunction in neuronal and neuroimmune populations causes MCHS-like behaviors in mice, highlighting its role in brain development and function.

bioRxiv · Oct 30, 2019 · PreprintNeuroscience