This study suggests that polyG protein aggregates in NIID may shift the global RNA splicing profile toward an immature state, potentially through the sequestration of key splicing factors, such as SF3B4, thereby identifying new avenues for understanding the pathogenic mechanisms underlying NIID.
Neuronal Intranuclear Inclusion Disease (NIID) is caused by GGC repeat expansions in the 5' untranslated region of the notch 2 N-terminal like C (NOTCH2NLC) gene. An upstream open reading frame within the mutant transcript produces the NOTCH2NLC upstream open reading frame-derived polyglycine protein (uN2CpolyG) contai...
Arisa Kubokawa, Ai Ohki, Risa Ono et al.· Biological and Pharmaceutica...· 0 citations
Proteostasis failure drives multiple neurodegenerative disorders (NDs), and ATP-independent chaperone pathways that support neuronal proteostasis remain poorly defined. Here, we identify the N6-methyladenosine (m6A)-binding protein YTHDC1 as an ATP-independent molecular chaperone, whose activity is mediated by a highly...
Kang Ren, Ming-Jie Cheng, Qiudan Luo et al.· Nature Communications· 0 citations
Using a combination of biochemical assays, structural modeling and molecular dynamics, it is shown that TTC33 directly recruits WDR61 and PHF5A to assemble into a trimeric core complex (TANC), which then forms distinct interactions with either UNG1/2 or SF3B–CCDC97.
R. Tomecki, Małgorzata Drabko, Małgorzata Siek et al.· Nature Communications· 0 citations
The U1 small nuclear ribonucleoprotein (U1 snRNP) is an essential spliceosome component that mediates pre-mRNA splicing. Although the molecular function of Luc7 proteins is broadly conserved in eukaryotes, whether this core splicing factor acquires developmentally specialized functions in filamentous fungi remains uncl...
Jie Wang, Ling Yang, En-Hui Bai et al.· International Journal of Bio...· 0 citations
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