Author

James W. Wheless

University of Tennessee Health Science Center

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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Genetics· 2

Signature Assays, Organisms & Methods

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Research Focus:differential expression· 2 Organism:human· 2 Approach:statistical model· 2 Research Focus:cell type annotation· 1 Assay:DNA methylation· 1 Organism:Drosophila· 1 Approach:experimental assay· 1 Research Focus:gene regulatory network inference· 1

Frequent Co-Authors

Alejandro D. IglesiasiD· 1 shared Alicia M. H. CaseyiD· 1 shared Andrew A. HardiganiD· 1 shared Angela BahriD· 1 shared Anita M. RauchiD· 1 shared Anna HurstiD· 1 shared Annick Raas‐RothschildiD· 1 shared Anya Revah‐PolitiiD· 1 shared

Activity by Year

2018-2020 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 20 mutual co-author links

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1 shared paperGenetics

Alejandro D. IglesiasORCID

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2 papers

Recent·Most cited

Characterization of SETD1A haploinsufficiency in humans and Drosophila defines a novel neurodevelopmental syndrome.

Joost Kummeling, Diante E. Stremmelaar, Nicholas Raun, Margot R.F. Reijnders, Marjolein H. Willemsen, Martina Ruiterkamp‐Versteeg, Marga T. Schepens, C Man, Christian Gilissen, Megan T. Cho, Kirsty M. McWalter, Margje Sinnema, James W. Wheless, Marleen Simon, Casie A. Genetti, , Tjitske Kleefstra

This study characterizes SETD1A haploinsufficiency in humans and Drosophila, identifying a novel neurodevelopmental syndrome with cognitive and developmental symptoms.

Molecular Psychiatry · Apr 28, 2020Peer-reviewedGenetics

De novo mutations in the GTP/GDP-binding region of RALA, a RAS-like small GTPase, cause intellectual disability and developmental delay

Susan M. Hiatt, Matthew B. Neu, Ryne C. Ramaker, Andrew A. Hardigan, Jeremy W. Prokop, Miroslava Hančárová, Darina Prchalová, Markéta Havlovičová, Jan Prchal, Viktor Stránecký, Dwight K. C. Yim, Zöe Powis, Boris Keren, Caroline Nava, Cyril Mignot, , Gregory M. Cooper

The paper identifies de novo mutations in RALA, a RAS-like GTPase, as a cause of intellectual disability and developmental delay, showing their functional impact on GTP binding and effector interactions.

PLoS Genetics · Nov 30, 2018Peer-reviewedGenetics