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TDP-43 nuclear loss in FTD-ALS causes widespread alternative polyadenylation

GSE252892 Homo sapiens Expression profiling by high throughput sequencing; Other 12 samples 2025/11/20 GPL30173
Summary
In frontotemporal dementia and amyotrophic lateral sclerosis, the RNA-binding protein TDP-43 is depleted from the nucleus. TDP-43 loss leads to cryptic exon inclusion but a role in other RNA processing events remains unresolved. Here, we show that loss of TDP-43 causes widespread changes in alternative polyadenylation, impacting expression of disease-relevant genes (e.g., ELP1, NEFL, and TMEM106B), providing evidence that alternative polyadenylation is a new facet to TDP-43 pathology.
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NCBI GEO page ↗ Paper (PMID 41120750) ↗ {# Names what the click gives you. "Open in finder" meant nothing to a visitor who arrived from a search engine and has never seen the tool. #} Find more human RNA-seq datasets →
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