L
Leslie M. Thompson
Researcher at University of California, Irvine
Publications - 168
Citations - 33671
Leslie M. Thompson is an academic researcher from University of California, Irvine. The author has contributed to research in topics: Huntingtin & Huntington's disease. The author has an hindex of 65, co-authored 149 publications receiving 31173 citations. Previous affiliations of Leslie M. Thompson include University of California, Berkeley.
Papers
More filters
Journal ArticleDOI
A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes
Marcy E. MacDonald,Christine Ambrose,Mabel P. Duyao,Richard H. Myers,Carol Lin,Lakshmi Srinidhi,Glenn Barnes,Sherryl A.M. Taylor,Marianne James,Nicolet Groot,Heather MacFarlane,Barbara Jenkins,Mary Anne Anderson,Nancy S. Wexler,James F. Gusella,Gillian P. Bates,Sarah Baxendale,Holger Hummerich,Susan F. Kirby,Mike North,S. Youngman,Richard Mott,Günther Zehetner,Zdenek Sedlacek,Annemarie Poustka,Anna-Maria Frischauf,Hans Lehrach,Alan Buckler,Deanna M. Church,Lynn Doucette-Stamm,Michael Conlon O'Donovan,Laura Riba-Ramirez,Manish A. Shah,Vincent P. Stanton,Scott A. Strobel,Karen M. Draths,Jennifer L. Wales,Peter B. Dervan,David E. Housman,Michael R. Altherr,Rita Shiang,Leslie M. Thompson,Thomas J. Fielder,John J. Wasmuth,Danilo A. Tagle,John Valdes,Lawrence W. Elmer,Marc W. Allard,Lucio H. Castilla,Manju Swaroop,Kris Blanchard,Francis S. Collins,Russell G. Snell,Tracey Holloway,Kathleen Gillespie,Nicole A. Datson,Duncan Shaw,Peter S. Harper +57 more
TL;DR: In this article, the authors used haplotype analysis of linkage disequilibrium to spotlight a small segment of 4p16.3 as the likely location of the defect, which is expanded and unstable on HD chromosomes.
Journal Article
A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes. The Huntington's Disease Collaborative Research Group.
Manish A. Shah,Nicole A. Datson,Lakshmi Srinidhi,Vincent P. Stanton,Marcy E. MacDonald,Marc W. Allard,S. Youngman,Anna-Maria Frischauf,Richard Mott,KM Draths,Günther Zehetner,C. O’Donovan,Thomas J. Fielder,Bruce G. Jenkins,Manju Swaroop,Sherryl A.M. Taylor,Lynn Doucette-Stamm,Heather MacFarlane,Scott A. Strobel,H. E. McFarlane,Alan Buckler,Nicolet Groot,Holger Hummerich,Deanna M. Church,M. A. Anderson,Marianne James,Glenn Barnes,M. Christine,Francis S. Collins,Mabel P. Duyao,Peter B. Dervan,Gillian P. Bates,T Holloway,Peter S. Harper,TW Mcdonald,M North,K Blanchard,John J. Wasmuth,D. Shaw,Hans Lehrach,Danilo A. Tagle,Annemarie Poustka,David E. Housman,T. Huntington,Zdenek Sedlacek,Laura Riba,Susan F. Kirby,Carol Lin,Richard H. Myers,Leslie M. Thompson,Russell G. Snell,Michael Conlon O'Donovan,K Gillespie,Rita Shiang,Nancy S. Wexler,Christine Ambrose,J. F. Gusella,Sarah Baxendale,N. Groat,John Valdes +59 more
TL;DR: The Huntington's disease mutation involves an unstable DNA segment, similar to those described in fragile X syndrome, spino-bulbar muscular atrophy, and myotonic dystrophy, acting in the context of a novel 4p16.3 gene to produce a dominant phenotype.
Journal ArticleDOI
Histone deacetylase inhibitors arrest polyglutamine-dependent neurodegeneration in Drosophila
Joan S. Steffan,László Bodai,Judit Pallos,Marnix Poelman,Alexander McCampbell,Barbara L. Apostol,Alexsey Kazantsev,Emily Schmidt,Ya-Zhen Zhu,Marilee Greenwald,Riki Kurokawa,David E. Housman,George R. Jackson,J. Lawrence Marsh,Leslie M. Thompson +14 more
TL;DR: It is shown that the polyglutamine-containing domain of Htt, Htt exon 1 protein (Httex1p), directly binds the acetyltransferase domains of two distinct proteins: CREB-binding protein (CBP) and p300/CBP-associated factor (P/CAF).
Journal ArticleDOI
Mutations in the transmembrane domain of FGFR3 cause the most common genetic form of dwarfism, achondroplasia.
Rita Shiang,Leslie M. Thompson,Ya-Zhen Zhu,Deanna M. Church,Thomas J. Fielder,Maureen Bocian,Sara T. Winokur,John J. Wasmuth +7 more
TL;DR: DNA studies revealed point mutations in the FGFR3 gene in ACH heterozygotes and homozygotes, which result in the substitution of an arginine residue for a glycine at position 380 of the mature protein, which is in the transmembrane domain ofFGFR3.
Journal ArticleDOI
The Huntington's disease protein interacts with p53 and CREB-binding protein and represses transcription.
Joan S. Steffan,Aleksey G. Kazantsev,Olivera Spasic-Boskovic,Marilee Greenwald,Ya-Zhen Zhu,Heike Göhler,Erich E. Wanker,Gillian P. Bates,David E. Housman,Leslie M. Thompson +9 more
TL;DR: The possibility that expanded repeat htt causes aberrant transcriptional regulation through its interaction with cellular transcription factors which may result in neuronal dysfunction and cell death in HD is raised.