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TDP-43 protein loss in neurons induces widespread changes in polyadenylation, possibly explaining its role in causing ALS/FTD beyond its known role in cryptic exon regulation. doi.org/qgd5 doi.org/hbctcv
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Loss of TDP-43 from cell nuclei in ALS and FTD disrupts alternative polyadenylation, altering gene expression and protein production in neurons. This mechanism may inform future therapeutic strategies. doi.org/hbctcv
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ALS and frontotemporal dementia share a key molecular feature: dysfunction of the TDP-43 protein, which disrupts RNA processing and may inform future diagnostics and therapeutic strategies. doi.org/hbctcv
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Two separate studies from Gitler & Fratta labs reveal nuclear loss of TDP-43 disrupts RNA processing by altering alternative 3′ end cleavage & polyadenylation. They uncover new molecular signatures & shed new light on TDP-43 pathology www.nature.com/artic…