BLOG > Publications & Citations > TBK1 eliminates monomeric TDP-43 via an IFNβ-immunoproteasome pathway in ALS
Authors: Sakai, S., Oiwa, K., Iguchi, Y. et al.
Source: EMBO Rep (2026).
We're delighted to share insights from a recent study entitled "TBK1 eliminates aggregation-prone monomeric TDP-43 through an IFNβ-immunoproteasome pathway in ALS models" published in EMBO Reports by Shohei Sakai et al.
They identified a TBK1-IFNβ-immunoproteasome axis as a novel autophagy-independent proteostatic pathway regulating TDP-43 clearance. TBK1 is activated by aggregation-prone monomeric TDP-43 via physical association, subsequently inducing IFNβ expression, which upregulates the immunoproteasome to promote degradation of monomeric TDP-43 in neurons. IFNβ receptor expression was found to be downregulated in spinal motor neurons from ALS patients with TDP-43 pathology, and heterozygous Tbk1 deletion in SOD1G93A mice impaired immunoproteasome induction, supporting the in vivo relevance of this pathway.
Congratulations to all authors for this great article.
NeuroMag was used to transfect iPSC-derived lower motor neurons at induction day 10 with plasmid DNA to investigate TDP-43 pathology in a human neuronal model.
Read the article Access NeuroMag
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