Neuronal Puncta/Aggregate Formation by WT and Mutant UBQLN2
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Publisher
Springer US
Link
https://link.springer.com/content/pdf/10.1007/978-1-0716-2597-2_34
Reference17 articles.
1. Deng H-X, Chen W, Hong S-T et al (2011) Mutations in UBQLN2 cause dominant X-linked juvenile and adult-onset ALS and ALS/dementia. Nature 477(7363):211–215. https://doi.org/10.1038/nature10353
2. Williams KL, Warraich ST, Yang S et al (2012) UBQLN2/ubiquilin 2 mutation and pathology in familial amyotrophic lateral sclerosis. Neurobiol Aging 33(10):2527.e3–2527.e10. https://doi.org/10.1016/j.neurobiolaging.2012.05.008
3. Teyssou E, Chartier L, Amador MDM et al (2017) Novel UBQLN2 mutations linked to amyotrophic lateral sclerosis and atypical hereditary spastic paraplegia phenotype through defective HSP70-mediated proteolysis. Neurobiol Aging 58:239.e11–239.e20. https://doi.org/10.1016/j.neurobiolaging.2017.06.018
4. Gkazi SA, Troakes C, Topp S et al (2019) Striking phenotypic variation in a family with the P506S UBQLN2 mutation including amyotrophic lateral sclerosis, spastic paraplegia, and frontotemporal dementia. Neurobiol Aging 73:229.e5–229.e9. https://doi.org/10.1016/j.neurobiolaging.2018.08.015
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1. Stress granule formation helps to mitigate neurodegeneration;Nucleic Acids Research;2024-08-06
2. Pathogenic mutations in UBQLN2 exhibit diverse aggregation propensity and neurotoxicity;Scientific Reports;2024-03-13
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