J
Jessica L. Walcott
Researcher at Thomas Jefferson University
Publications - 5
Citations - 1042
Jessica L. Walcott is an academic researcher from Thomas Jefferson University. The author has contributed to research in topics: Spinal and bulbar muscular atrophy & Trinucleotide repeat expansion. The author has an hindex of 5, co-authored 5 publications receiving 1020 citations. Previous affiliations of Jessica L. Walcott include University of Pennsylvania.
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Journal ArticleDOI
CREB-binding protein sequestration by expanded polyglutamine
Alexander McCampbell,J. Paul Taylor,Addis A. Taye,Jon Robitschek,Mei Li,Jessica L. Walcott,Diane E. Merry,Yaohui Chai,Henry L. Paulson,Gen Sobue,Kenneth H. Fischbeck +10 more
TL;DR: Evidence is presented that CREB-binding protein (CBP), a transcriptional co-activator that orchestrates nuclear response to a variety of cell signaling cascades, is incorporated into nuclear inclusions formed by polyglutamine-containing proteins in cultured cells, transgenic mice and tissue from patients with SBMA.
Journal ArticleDOI
Altered Trafficking of Mutant Connexin32
Suzanne M. Deschênes,Jessica L. Walcott,Tamara Wexler,Steven S. Scherer,Kenneth H. Fischbeck +4 more
TL;DR: It is suggested that diseases affecting myelinating cells may share a common pathophysiology and CMTX mutations have a predominant effect on the trafficking of Cx32 protein, resulting in a potentially toxic cytoplasmic accumulation of C x32 in these cells.
Journal ArticleDOI
Expression of expanded repeat androgen receptor produces neurologic disease in transgenic mice
TL;DR: The development of transgenic mice, created with a truncated, highly expanded androgen receptor driven by the neurofilament light chain promoter, which develop many of the motor symptoms of SBMA and the other polyglutamine diseases, and neuronal intranuclear inclusions (NIIs) are shown to be ubiquitinated.
Journal ArticleDOI
Ligand promotes intranuclear inclusions in a novel cell model of spinal and bulbar muscular atrophy.
TL;DR: This model mimics the formation of ubiquitinated intranuclear inclusions containing the amino-terminal portion of AR observed in patient tissue and reveals a role for ligand in the pathogenesis of SBMA.
Book ChapterDOI
Trinucleotide repeat disease. The androgen receptor in spinal and bulbar muscular atrophy.
TL;DR: In this article, the expansion of a simple CAG trinucleotide repeat within the coding region of the androgen receptor gene leads to the motor neuronopathy spinal and bulbar muscular atrophy (SBMA).