Associated Papers
Defining RNA oligonucleotides that reverse deleterious phase transitions of RNA-binding proteins with prion-like domains.
Guo L et al.
Molecular Cell, 2026
Intra-condensate demixing of TDP-43 inside stress granules generates pathological aggregates.
Yan X et al.
Cell, 2025
Defining RNA oligonucleotides that reverse deleterious phase transitions of RNA-binding proteins with prion-like domains.
Guo L et al.
Biorxiv : the Preprint Server for Biology, 2023
Impaired RNA Binding Does Not Prevent Histone Modification Changes in a FUS ALS/FTD Yeast Model.
Bennett SA et al.
Micropublication Biology, 2023
DDX17 is involved in DNA damage repair and modifies FUS toxicity in an RGG-domain dependent manner.
Fortuna TR et al.
Acta Neuropathologica, 2021
Nuclear egress of TDP-43 and FUS occurs independently of Exportin-1/CRM1.
Ederle H et al.
Scientific Reports, 2018
U1 snRNP is mislocalized in ALS patient fibroblasts bearing NLS mutations in FUS and is required for motor neuron outgrowth in zebrafish.
Yu Y et al.
Nucleic Acids Research, 2015
Functions of FUS/TLS from DNA repair to stress response: implications for ALS.
Sama RR et al.
Asn Neuro, 2014
ALS-associated FUS mutations result in compromised FUS alternative splicing and autoregulation.
Zhou Y et al.
Plos Genetics, 2013
RNA-binding ability of FUS regulates neurodegeneration, cytoplasmic mislocalization and incorporation into stress granules associated with FUS carrying ALS-linked mutations.
Daigle JG et al.
Human Molecular Genetics, 2013
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