ArticleCells2018
Perturbations in Traffic: Aberrant Nucleocytoplasmic Transport at the Heart of Neurodegeneration.
Article in Cells, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- FOXO family and neurodegenerative diseases: Mechanisms of action and therapeutic potential.Redox biology · 2026Review
- Review of the Pathology of Muscle in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2026Review
- Nup358 restricts ER-mitochondria connectivity by modulating mTORC2/Akt/GSK3β signalling.EMBO reports · 2024Article
- Endosome mediated nucleocytoplasmic trafficking and endomembrane allocation is crucial to polyglutamine toxicity.Cell biology and toxicology · 2024Article
- Kinetic cooperativity resolves bidirectional clogging within the nuclear pore complex.Biophysical journal · 2024Article
- Modeling sporadic juvenile ALS in iPSC-derived motor neurons explores the pathogenesis of FUSFrontiers in cellular neuroscience · 2024Article
- Hypoxia-Induced FUS-circTBC1D14 Stress Granules Promote Autophagy in TNBC.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Self-regulation of the nuclear pore complex enables clogging-free crowded transport.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Hsp70 exhibits a liquid-liquid phase separation ability and chaperones condensed FUS against amyloid aggregation.iScience · 2022Article
- Review
- First record on mercury accumulation in mice brain living in active volcanic environments: a cytochemical approach.Environmental geochemistry and health · 2021Article
- Abnormal scaffold attachment factor 1 expression and localization in spinocerebellar ataxias and Huntington's chorea.Brain pathology (Zurich, Switzerland) · 2020Article
- The hippo kinase STK38 ensures functionality of XPO1.Cell cycle (Georgetown, Tex.) · 2020Review
- The Nuclear Lamina: Protein Accumulation and Disease.Biomedicines · 2020Review
- Quantitative Nucleocytoplasmic Transport Assays in Cellular Models of Neurodegeneration.Bio-protocol · 2020Article
- Autophagy in aging and longevity.Human genetics · 2020Review
- Nuclear Transport Deficits in Tau-Related Neurodegenerative Diseases.Frontiers in neurology · 2020Review
- Tau oligomers mediate aggregation of RNA-binding proteins Musashi1 and Musashi2 inducing Lamin alteration.Aging cell · 2019Article
- Pathogenic Variants in NUP214 Cause "Plugged" Nuclear Pore Channels and Acute Febrile Encephalopathy.American journal of human genetics · 2019Article
- Disrupted neuronal trafficking in amyotrophic lateral sclerosis.Acta neuropathologica · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Neurodegenerative diseases, such as amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and Huntington's disease (HD), are characterized by intracellular aggregation of proteins. In the case of ALS and FTD, these protein aggregates are found in the cytoplasm of affected neurons and contain certain RNA-binding proteins (RBPs), namely the TAR DNA-binding protein of 43 kDa (TDP-43) and the fused in sarcoma (FUS) gene product. TDP-43 and FUS are nuclear proteins and their displacement to the cytoplasm is thought to be adverse in at least two ways: loss-of-function in the nucleus and gain-of-toxicity in the cytoplasm. In the case of HD, expansion of a polyglutamine (polyQ) stretch within the N-terminal domain of the Huntingtin (HTT) protein leads to nuclear accumulation of polyQ HTT (or mHTT) and a toxic gain-of-function phenotype resulting in neurodegeneration. Numerous studies in recent years have provided evidence that defects in nucleocytoplasmic transport critically contribute to the pathology of these neurodegenerative diseases. A new mechanistic view is emerging, implicating three types of perturbations in normal cellular pathways that rely on nucleocytoplasmic transport: displacement of nuclear transport receptors and nucleoporins from nuclear pore complexes (NPCs), mislocalization and aggregation of RNA-binding proteins, and weakening of the chaperone activity of nuclear import receptors.
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What OpenQuestion holds
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.