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Yong-hui Jiang
Researcher at Duke University
Publications - 152
Citations - 14253
Yong-hui Jiang is an academic researcher from Duke University. The author has contributed to research in topics: Autism & Exome sequencing. The author has an hindex of 47, co-authored 143 publications receiving 12372 citations. Previous affiliations of Yong-hui Jiang include Howard Hughes Medical Institute & University of Pittsburgh.
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Journal ArticleDOI
Molecular classification of cutaneous malignant melanoma by gene expression profiling
M. Bittner,Paul S. Meltzer,Yi Chen,Yong-hui Jiang,E. A. Seftor,Mary J.C. Hendrix,Michael D. Radmacher,Richard M. Simon,Zohar Yakhini,Amir Ben-Dor,Amir Ben-Dor,Nick Sampas,Edward R. Dougherty,Ena Wang,Francesco M. Marincola,C. Gooden,John Lueders,Arthur A. Glatfelter,P.C.A. Pollock,John D. Carpten,E. Gillanders,D. Leja,K. Dietrich,Christian Beaudry,Michael E. Berens,David S. Alberts,Vernon K. Sondak,Nicholas K. Hayward,J.M. Trent +28 more
TL;DR: Many genes underlying the classification of this subset of melanomas are differentially regulated in invasive melanomas that form primitive tubular networks in vitro, a feature of some highly aggressive metastatic melanomas.
Journal ArticleDOI
De novo truncating mutations in E6-AP ubiquitin-protein ligase gene (UBE3A) in Angelman syndrome.
Toshinobu Matsuura,James S. Sutcliffe,Ping Fang,Robert-Jan Galjaard,Yong-hui Jiang,Claudia S. Benton,Johanna M. Rommens,Arthur L. Beaudet +7 more
TL;DR: Intragenic mutation of UBE3A in AS is the first examples of a genetic disorder of the ubiquitin-dependent proteolytic pathway in mammals and may represent an example of a human genetic disorder associated with a locus producing functionally distinct imprinted and biallelically expressed gene products.
Journal ArticleDOI
Mutation of the angelman ubiquitin ligase in mice causes increased cytoplasmic p53 and deficits of contextual learning and long-term potentiation
Yong-hui Jiang,Dawna L. Armstrong,Urs Albrecht,Coleen M. Atkins,Jeffrey L. Noebels,Gregor Eichele,J. D. Sweatt,Arthur L. Beaudet,Arthur L. Beaudet +8 more
TL;DR: The cytoplasmic abundance of p53 was increased in postmitotic neurons in m-/p+ mice and in AS, providing a potential biochemical basis for the phenotype through failure to ubiquitinate and degrade various effectors.
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Mutation of the E6-AP Ubiquitin Ligase Reduces Nuclear Inclusion Frequency While Accelerating Polyglutamine-Induced Pathology in SCA1 Mice
Christopher J. Cummings,Eyal Reinstein,Yaling Sun,Barbara Antalffy,Yong-hui Jiang,Aaron Ciechanover,Harry T. Orr,Arthur L. Beaudet,Huda Y. Zoghbi +8 more
TL;DR: In mice, Purkinje cells that express mutant ataxin-1 but not a ubiquitin-protein ligase have significantly fewer NIs, and in mice, the Purkinjen cell pathology is markedly worse than that of SCA1 mice.
Journal ArticleDOI
Synaptic dysfunction and abnormal behaviors in mice lacking major isoforms of Shank3
Xiaoming Wang,Portia A. McCoy,Ramona M. Rodriguiz,Yanzhen Pan,H. Shawn Je,Adam C. Roberts,Caroline J. Kim,Janet Berrios,Jennifer S. Colvin,Danielle Bousquet-Moore,Isabel Lorenzo,Gang Yi Wu,Richard J. Weinberg,Michael D. Ehlers,Michael D. Ehlers,Benjamin D. Philpot,Arthur L. Beaudet,William C. Wetsel,Yong-hui Jiang +18 more
TL;DR: It is concluded that loss of major Shank3 species produces biochemical, cellular and morphological changes, leading to behavioral abnormalities in mice that bear similarities to human ASD patients with SHANK3 mutations.