TDP-43 nuclear loss in FTD/ALS causes widespread alternative polyadenylation changes
Zeng, Y.; Lovchykova, A.; Aikyama, T.; Liu, C.; Guo, C.; Jawahar, V. M.; Sianto, O.; Calliari, A.; Prudencio, M.; Dickson, D. W.; Petrucelli, L.; Gitler, A. D.
Show abstract
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) and providing evidence that alternative polyadenylation is a new facet of TDP-43 pathology.
Matching journals
The top 3 journals account for 50% of the predicted probability mass.
Similar papers in this journal
Similar papers in this journal
- Transfer RNA acetylation regulates in vivo mammalian stress signaling 95%
- Integrated single-cell transcriptomic and epigenetic analyses of cell-state transition and lineage commitment in the embryonic mouse cerebellum 95%
- Antagonistic H3K79me-H3K9ac crosstalk determines elongation at housekeeping genes to promote pluripotency 95%
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.