Associated Papers
Transcriptomic Alteration in FUS-ALS Points Towards Apoptosis-Rather than Ferroptosis-Related Cell Death Pathway.
Dash BP et al.
Cells, 2025
Single-cell RNA-sequencing reveals early mitochondrial dysfunction unique to motor neurons shared across FUS- and TARDBP-ALS.
Schweingruber C et al.
Nature Communications, 2025
40389397 (PubMed )
Supplement: 41467_2025_59679_MOESM3_ESM.xlsx › FUS_Clinical_Data
Multiomics and machine-learning identify novel transcriptional and mutational signatures in amyotrophic lateral sclerosis.
Catanese A et al.
Brain : a Journal of Neurology, 2023
Integrative proteomics highlight presynaptic alterations and c-Jun misactivation as convergent pathomechanisms in ALS.
Aly A et al.
Acta Neuropathologica, 2023
Characterising the Genetic Landscape of Amyotrophic Lateral Sclerosis: A Catalogue and Assessment of Over 1,000 Published Genetic Variants.
McCann EP et al.
Journal of Neuromuscular Diseases, 2023
37638449 (PubMed )
Supplement: jnd-10-jnd230148-s001.xlsx › variant_list
FUS-mediated regulation of acetylcholine receptor transcription at neuromuscular junctions is compromised in amyotrophic lateral sclerosis.
Picchiarelli G et al.
Nature Neuroscience, 2019
The role of de novo mutations in adult-onset neurodegenerative disorders.
Nicolas G et al.
Acta Neuropathologica, 2019
30478624 (PubMed )
Supplement: 401_2018_1939_MOESM1_ESM.xlsx › Supp_Table_2_FTLD_spectrum
ALS-causing mutations differentially affect PGC-1α expression and function in the brain vs. peripheral tissues.
Bayer H et al.
Neurobiology of Disease, 2017
FUS Mislocalization and Vulnerability to DNA Damage in ALS Patients Derived hiPSCs and Aging Motoneurons.
Higelin J et al.
Frontiers in Cellular Neuroscience, 2016
De novo FUS mutations are the most frequent genetic cause in early-onset German ALS patients.
Hübers A et al.
Neurobiology of Aging, 2015
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