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Stress Granule Assembly Disrupts Nucleocytoplasmic Transport
Zhang K, Daigle JG, Cunningham KM, Coyne AN, Ruan K, Grima JC, Bowen KE, Wadhwa H et al.. Cell, 2018-04-05
Topic: Brain proteins, microglia and lab models
Defects in nucleocytoplasmic transport have been identified as a key pathogenic event in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) mediated by a GGGGCC hexanucleotide repeat expansion in C9ORF72, the most common genetic cause of ALS/FTD. Furthermore, nucleocytoplasmic transport disruption has also been implicated in other neurodegenerative diseases with protein aggregation, suggesting a shared mechanism by which protein stress disrupts nucleocytoplasmic transport. Here, we show that cellular stress disrupts nucleocytoplasmic transport by localizing critical nucleocytoplasmic transport factors into stress granules, RNA/protein complexes that play a crucial role in ALS pathogenesis. Importantly, inhibiting stress granule assembly, such as by knocking down Ataxin-2, suppresses nucleocytoplasmic transport defects as well as neurodegeneration in C9ORF72-mediated ALS/FTD. Our findings identify a link between stress granule assembly and nucleocytoplasmic transport, two fundamental cellular processes implicated in the pathogenesis of C9ORF72-mediated ALS/FTD and other neurodegenerative diseases.
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APA 7th
Zhang, K., Daigle, J. G., Cunningham, K. M., Coyne, A. N., Ruan, K., Grima, J. C., et al. (2018). Stress Granule Assembly Disrupts Nucleocytoplasmic Transport. Cell. https://doi.org/10.1016/j.cell.2018.03.025
Vancouver
Zhang K, Daigle JG, Cunningham KM, Coyne AN, Ruan K, Grima JC, et al. Stress Granule Assembly Disrupts Nucleocytoplasmic Transport. Cell. 2018. doi:10.1016/j.cell.2018.03.025. PMID: 29628143.
BibTeX
@article{zhang2018-29628143,
author = {Zhang, K. and Daigle, J. G. and Cunningham, K. M. and Coyne, A. N. and Ruan, K. and Grima, J. C. and Bowen, K. E. and Wadhwa, H. and others},
title = {{Stress Granule Assembly Disrupts Nucleocytoplasmic Transport}},
journal = {Cell},
year = {2018},
doi = {10.1016/j.cell.2018.03.025},
pmid = {29628143},
url = {https://doi.org/10.1016/j.cell.2018.03.025}
}
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Key findings
- Our findings identify a link between stress granule assembly and nucleocytoplasmic transport, two fundamental cellular processes implicated in the pathogenesis of C9ORF72-mediated ALS/FTD and other neurodegenerative diseases.
Why it matters
This laboratory work found that cellular stress disrupts nucleocytoplasmic transport by moving transport factors into stress granules, and that blocking stress granule assembly reduced these defects and neurodegeneration in C9ORF72-mediated ALS/FTD. It is cell and model research, so it does not yet show any treatment, cure or prevention for Alzheimer's disease.
Study details
- Evidence strengthLow
How this study scored 55/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Cell) |
| Journal's citation record | 4 / 4 | Cell: journal h-index 1,220 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 2 / 5 | 2018 — within 10 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 6 / 7 | Cited 424 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 42.4 citations a year over 10 year(s) since 2018 |
| Impact for its field and year | 5 / 6 | Cited 30.8× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 13 other studies in this library |
| Still being cited | 3 / 4 | Cited 117 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Thomas E. Lloyd: h-index 53 (OpenAlex, whole career) |
| Institution's track record | 3 / 3 | Stanford University: institution h-index 2,684 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 7 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 29628143) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 55 / 100 | — |
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