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PRODID:-//Department of Neuroscience//NONSGML Events//EN
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X-ORIGINAL-URL:https://neuroscience.wustl.edu/events/
X-WR-CALDESC:Department of Neuroscience - Events
BEGIN:VEVENT
UID:20251119T2044Z-1763585049.029-EO-25965-1@10.73.9.33
STATUS:CONFIRMED
DTSTAMP:20260717T004421Z
CREATED:20251119T204100Z
LAST-MODIFIED:20260129T151442Z
DTSTART;TZID=America/Chicago:20260204T120000
DTEND;TZID=America/Chicago:20260204T130000
SUMMARY: Department of Neuroscience Seminar: Frederick Arnold\, PhD (WashU 
 Medicine)
DESCRIPTION: Frederick Arnold is giving a Department of Neuroscience Semina
 r talk at WashU Medicine.
X-ALT-DESC;FMTTYPE=text/html: <h3><strong>"Identifying new biomarkers and t
 herapeutic targets for TDP-43 proteinopathies"</strong></h3><p><a href="htt
 ps://genetics.wustl.edu/people/frederick-arnold-phd/">Frederick Arnold\, Ph
 D<img class="size-medium wp-image-25966 alignright" src="https://neuroscien
 ce.wustl.edu/app/uploads/2025/11/Frederick-Arnold-245x300.jpg" alt="Frederi
 ck Arnold is a man with short hair and wearing a blue plaid shirt." width="
 245" height="300" /></a><br />Assistant Professor of Genetics<br />WashU Me
 dicine</p><p>Nuclear depletion and cytoplasmic aggregation of the RNA-bindi
 ng protein TDP-43 are defining features of amyotrophic lateral sclerosis (A
 LS) and frontotemporal dementia (FTD). While TDP-43–dependent splicing regu
 lation is well established\, its role in alternative polyadenylation (APA) 
 and 3′ untranslated region (3′UTR) regulation was comparatively understudie
 d until recently. Using RNA-seq datasets from multiple cellular models of T
 DP-43 dysfunction\, combined with neuronal nuclei isolated from postmortem 
 ALS and FTD cortex\, we found that loss of nuclear TDP-43 resulted in wides
 pread shifts in polyadenylation site usage\, affecting hundreds of genes. T
 hese changes were highly enriched among transcripts directly bound by TDP-4
 3 and were characterized predominantly by increased use of distal polyadeny
 lation sites\, leading to 3′UTR lengthening.</p><p>By characterizing this n
 ew category of TDP-43-regulated genes\, we have uncovered several new bioma
 rker and therapeutic targets for ALS/FTD and other ‘TDP-43 proteinopathies\
 ,’ we were are actively investigating in the lab.</p>
CATEGORIES:Seminar Series
LOCATION:Neuroscience Research Building Auditorium
GEO:38.635602;-90.254892
ORGANIZER;CN="Shea":MAILTO:shea.stewart@wustl.edu
URL;VALUE=URI:https://neuroscience.wustl.edu/events/event/department-of-neu
 roscience-seminar-frederick-arnold/
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TZID:America/Chicago
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TZOFFSETFROM:-0500
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DTSTART:20251102T070000
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