ReviewInternational journal of molecular sciences2021
The Role of Nucleocytoplasmic Transport Defects in Amyotrophic Lateral Sclerosis.
Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
- Sex-Related Differences in Circular RNA Expression in Multiple Sclerosis: A Pilot Study.Journal of molecular neuroscience : MN · 2026Article
- Neuronal Cell-Cycle Re-entry Defines Divergent Outcomes Through Replication-Dependent DNA Damage in ALS.bioRxiv : the preprint server for biology · 2026Article
- Article
- Review
- Ibetazol, a novel inhibitor of importin β1-mediated nuclear import.Communications biology · 2024Article
- Understanding Amyotrophic Lateral Sclerosis: Pathophysiology, Diagnosis, and Therapeutic Advances.International journal of molecular sciences · 2024Review
- Mitochondrial Dysfunction in Sporadic Amyotrophic Lateral Sclerosis Patients: Insights from High-Resolution Respirometry.Biomedicines · 2024Article
- A comparison study of pathological features and drug efficacy between Drosophila models of C9orf72 ALS/FTD.Molecules and cells · 2024Article
- Review
- Molecular Chaperones' Potential against Defective Proteostasis of Amyotrophic Lateral Sclerosis.Cells · 2023Review
- Proteomics Analysis of Lymphoblastoid Cell Lines from Patients with Amyotrophic Lateral Sclerosis.Molecules (Basel, Switzerland) · 2023Article
- Cellular Stress Induces Nucleocytoplasmic Transport Deficits Independent of Stress Granules.Biomedicines · 2022Article
- Article
- Emerging Connections between Nuclear Pore Complex Homeostasis and ALS.International journal of molecular sciences · 2022Review
- Measuring and Interpreting Nuclear Transport in Neurodegenerative Disease-The Example of C9orf72 ALS.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is ample evidence that nucleocytoplasmic-transport deficits could play an important role in the pathology of amyotrophic lateral sclerosis (ALS). However, the currently available data are often circumstantial and do not fully clarify the exact causal and temporal role of nucleocytoplasmic transport deficits in ALS patients. Gaining this knowledge will be of great significance in order to be able to target therapeutically nucleocytoplasmic transport and/or the proteins involved in this process. The availability of good model systems to study the nucleocytoplasmic transport process in detail will be especially crucial in investigating the effect of different mutations, as well as of other forms of stress. In this review, we discuss the evidence for the involvement of nucleocytoplasmic transport defects in ALS and the methods used to obtain these data. In addition, we provide an overview of the therapeutic strategies which could potentially counteract these defects.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.