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. Author manuscript; available in PMC: 2024 Feb 5.
Published in final edited form as: Sci Transl Med. 2024 Jan 17;16(730):eadf9735. doi: 10.1126/scitranslmed.adf9735

Fig. 3. Insoluble TMEM106B interactome gives mechanistic insight into the role of TMEM106B deposition in disease pathogenesis for FTLD-TDP.

Fig. 3.

(A) Volcano plot of significantly enriched proteins that coimmunoprecipitated with TMEM106B from the sarkosyl-insoluble P3 fraction of nine FTLD-TDP CC/TT185 cases. Those with an adjusted P < 0.05 (cutoff marked by dashed line) are highlighted in red. (B and C) Top 10 GO Biological Process (B) and KEGG pathways (C) of significant hits in (A), sorted by fold enrichment. (D) STRING diagrams depicting proteins in the “endocytosis,”“ribosome,” and “pathways of neurodegeneration” KEGG pathways. Markov clustering (granularity/inflation parameter = 3) was used to visualize proteins with well-characterized functional relations in each pathway.