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• W2897722778 abstract "Abstract TDP-43 is the major disease protein associated with amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration with ubiquitinated inclusions (FTLD-TDP). Here we identify the transcriptional elongation factor Ell—a shared component of little elongation complex (LEC) and super elongation complex (SEC)—as a strong modifier of TDP-43-mediated neurodegeneration. Our data indicate select targets of LEC and SEC become upregulated in the fly ALS/FTLD-TDP model. Among them, U12 snRNA and a stress-induced long non-coding RNA Hsrω , functionally contribute to TDP-43-mediated degeneration. We extend the findings of Hsrω , which we identify as a chromosomal target of TDP-43, to show that the human orthologue Sat III is elevated in a human cellular disease model and FTLD-TDP patient tissue. We further demonstrate an interaction between TDP-43 and human ELL2 by co-immunoprecipitation from human cells. These findings reveal important roles of Ell-complexes LEC and SEC in TDP-43-associated toxicity, providing potential therapeutic insight for TDP-43-associated neurodegeneration." @default.
• W2897722778 created "2018-10-26" @default.
• W2897722778 creator A5006999330 @default.
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• W2897722778 date "2018-10-23" @default.
• W2897722778 modified "2023-10-16" @default.
• W2897722778 title "Aberrant activation of non-coding RNA targets of transcriptional elongation complexes contributes to TDP-43 toxicity" @default.
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• W2897722778 doi "https://doi.org/10.1038/s41467-018-06543-0" @default.
• W2897722778 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6199344" @default.
• W2897722778 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30353006" @default.
• W2897722778 hasPublicationYear "2018" @default.
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