OpenAlex Citation Counts

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OpenAlex is a bibliographic catalogue of scientific papers, authors and institutions accessible in open access mode, named after the Library of Alexandria. It's citation coverage is excellent and I hope you will find utility in this listing of citing articles!

If you click the article title, you'll navigate to the article, as listed in CrossRef. If you click the Open Access links, you'll navigate to the "best Open Access location". Clicking the citation count will open this listing for that article. Lastly at the bottom of the page, you'll find basic pagination options.

Requested Article:

Overriding FUS autoregulation in mice triggers gain-of-toxic dysfunctions in RNA metabolism and autophagy-lysosome axis
Shuo‐Chien Ling, Somasish Ghosh Dastidar, Seiya Tokunaga, et al.
eLife (2019) Vol. 8
Open Access | Times Cited: 80

Showing 1-25 of 80 citing articles:

ALS Genetics: Gains, Losses, and Implications for Future Therapies
Garam Kım, Olivia Gautier, Eduardo Tassoni-Tsuchida, et al.
Neuron (2020) Vol. 108, Iss. 5, pp. 822-842
Open Access | Times Cited: 292

The Overlapping Genetics of Amyotrophic Lateral Sclerosis and Frontotemporal Dementia
Yevgeniya Abramzon, Pietro Fratta, Bryan J. Traynor, et al.
Frontiers in Neuroscience (2020) Vol. 14
Open Access | Times Cited: 202

Mechanisms Regulating Muscle Regeneration: Insights into the Interrelated and Time-Dependent Phases of Tissue Healing
Laura Forcina, Marianna Cosentino, Antonio Musarò
Cells (2020) Vol. 9, Iss. 5, pp. 1297-1297
Open Access | Times Cited: 174

Amyotrophic lateral sclerosis caused by FUS mutations: advances with broad implications
Thomas G. Moens, Sandrine Da Cruz, Manuela Neumann, et al.
The Lancet Neurology (2025) Vol. 24, Iss. 2, pp. 166-178
Closed Access | Times Cited: 3

The role of hnRNPs in frontotemporal dementia and amyotrophic lateral sclerosis
Alexander Bampton, Lauren M. Gittings, Pietro Fratta, et al.
Acta Neuropathologica (2020) Vol. 140, Iss. 5, pp. 599-623
Open Access | Times Cited: 95

FUS ALS-causative mutations impair FUS autoregulation and splicing factor networks through intron retention
Jack Humphrey, Nicol Birsa, Carmelo Milioto, et al.
Nucleic Acids Research (2020) Vol. 48, Iss. 12, pp. 6889-6905
Open Access | Times Cited: 90

Neuroprotective effects of niclosamide on disease progression via inflammatory pathways modulation in SOD1-G93A and FUS-associated amyotrophic lateral sclerosis models
M Milani, Ilaria Della Valle, Simona Rossi, et al.
Neurotherapeutics (2024) Vol. 21, Iss. 3, pp. e00346-e00346
Open Access | Times Cited: 10

ALS/FTD mutations in UBQLN2 impede autophagy by reducing autophagosome acidification through loss of function
Josephine J. Wu, Ashley Cai, Jessie E. Greenslade, et al.
Proceedings of the National Academy of Sciences (2020) Vol. 117, Iss. 26, pp. 15230-15241
Open Access | Times Cited: 66

Implications of Selective Autophagy Dysfunction for ALS Pathology
Emiliano Vicencio, Sebastián Beltrán, Luis Labrador, et al.
Cells (2020) Vol. 9, Iss. 2, pp. 381-381
Open Access | Times Cited: 53

SETX (senataxin), the helicase mutated in AOA2 and ALS4, functions in autophagy regulation
P. Richard, Shuang Feng, Yueh-Lin Tsai, et al.
Autophagy (2020) Vol. 17, Iss. 8, pp. 1889-1906
Open Access | Times Cited: 51

Cytoplasmic FUS triggers early behavioral alterations linked to cortical neuronal hyperactivity and inhibitory synaptic defects
Jelena Scekic‐Zahirovic, Inmaculada Sanjuan-Ruiz, Vanessa W. Y. Kan, et al.
Nature Communications (2021) Vol. 12, Iss. 1
Open Access | Times Cited: 45

Disrupted autophagy and neuronal dysfunction in C. elegans knockin models of FUS amyotrophic lateral sclerosis
Saba N. Baskoylu, Natalie Chapkis, Burak Unsal, et al.
Cell Reports (2022) Vol. 38, Iss. 4, pp. 110195-110195
Open Access | Times Cited: 30

Role of RNA Binding Proteins with prion-like domains in muscle and neuromuscular diseases
Gina Picchiarelli, Luc Dupuis
Cell Stress (2020) Vol. 4, Iss. 4, pp. 76-91
Open Access | Times Cited: 48

The FUS gene is dual‐coding with both proteins contributing to FUS ‐mediated toxicity
Marie A. Brunet, Jean‐François Jacques, Sonya Nassari, et al.
EMBO Reports (2020) Vol. 22, Iss. 1
Open Access | Times Cited: 41

Modelling amyotrophic lateral sclerosis in rodents
Tiffany W. Todd, Leonard Petrucelli
Nature reviews. Neuroscience (2022) Vol. 23, Iss. 4, pp. 231-251
Closed Access | Times Cited: 24

Pathological insights from amyotrophic lateral sclerosis animal models: comparisons, limitations, and challenges
Longhong Zhu, Shihua Li, Xiao‐Jiang Li, et al.
Translational Neurodegeneration (2023) Vol. 12, Iss. 1
Open Access | Times Cited: 14

All Roads Lead to Rome: Different Molecular Players Converge to Common Toxic Pathways in Neurodegeneration
Shirel Argueti-Ostrovsky, Leenor Alfahel, Joy Kahn, et al.
Cells (2021) Vol. 10, Iss. 9, pp. 2438-2438
Open Access | Times Cited: 32

Where and Why Modeling Amyotrophic Lateral Sclerosis
Francesco Liguori, Susanna Amadio, Cinzia Volonté
International Journal of Molecular Sciences (2021) Vol. 22, Iss. 8, pp. 3977-3977
Open Access | Times Cited: 27

Emerging Roles for Phase Separation of RNA-Binding Proteins in Cellular Pathology of ALS
Katarina Miličević, Branislava Ranković, Pavle R. Anđjus, et al.
Frontiers in Cell and Developmental Biology (2022) Vol. 10
Open Access | Times Cited: 21

FUS Alters circRNA Metabolism in Human Motor Neurons Carrying the ALS-Linked P525L Mutation
Alessio Colantoni, Davide Capauto, Vincenzo Alfano, et al.
International Journal of Molecular Sciences (2023) Vol. 24, Iss. 4, pp. 3181-3181
Open Access | Times Cited: 11

Protein Aggregation and its Affecting Mechanisms in Neurodegenerative Diseases.
Junyun Wu, Jianan Wu, Tao Chen, et al.
Neurochemistry International (2024) Vol. 180, pp. 105880-105880
Closed Access | Times Cited: 4

Maintenance of neuronal TDP-43 expression requires axonal lysosome transport
Veronica H. Ryan, Sydney Lawton, Joel F. Reyes, et al.
(2025)
Open Access

Maintenance of neuronal TDP-43 expression requires axonal lysosome transport
Veronica H. Ryan, Sydney Lawton, Joel F. Reyes, et al.
(2025)
Open Access

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