Evidence map›Paper›PMID 30742233›Full record

ReviewCellular and molecular life sciences : CMLS2019

The coming-of-age of nucleocytoplasmic transport in motor neuron disease and neurodegeneration.

Paulo A Ferreira

Erratum issuedAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Nuclear transport proteins: structure, function, and disease relevance.Signal transduction and targeted therapy · 2023
    Review
  5. Review
  6. Article
  7. Article
  8. Sensory Involvement in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2022
    Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Widespread remodeling of proteome solubility in response to different protein homeostasis stresses.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  19. Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author.

Paulo A FerreiraDuke University Medical Center, DUEC 3802, 2351 Erwin Road, Durham, NC, 27710, USA. paulo.ferreira@duke.edu.ORCID http://orcid.org/0000-0003-4585-1717

Funding

STRUCTURE/FUNCTION ANALYSIS OF RANBP2 IN THE NEURORETINAR01EY011993 · NEI · MEDICAL COLLEGE OF WISCONSIN · PI FERREIRA, PAULO A · 1999 to 2006
$1.8M
Genetic and Molecular Analyses of Protein Biogenesis in the NeuroretinaR01EY019492 · NEI · DUKE UNIVERSITY · PI FERREIRA, PAULO A · 2010 to 2013
$1.5M
Genetic and Molecular Dissection of RanBP2-Mediated RanGTPase FunctionsR01GM083165 · NIGMS · DUKE UNIVERSITY · PI FERREIRA, PAULO A · 2010 to 2013
$1.4M
NEI NIH HHS EY019492NEI NIH HHS R01 EY011993NEI NIH HHS R01 EY019492NIGMS NIH HHS GM083165NIGMS NIH HHS R01 GM083165
6 · The paper itself

Abstract

The nuclear pore is the gatekeeper of nucleocytoplasmic transport and signaling through which a vast flux of information is continuously exchanged between the nuclear and cytoplasmic compartments to maintain cellular homeostasis. A unifying and organizing principle has recently emerged that cements the notion that several forms of amyotrophic lateral sclerosis (ALS), and growing number of other neurodegenerative diseases, co-opt the dysregulation of nucleocytoplasmic transport and that this impairment is a pathogenic driver of neurodegeneration. The understanding of shared pathomechanisms that underpin neurodegenerative diseases with impairments in nucleocytoplasmic transport and how these interface with current concepts of nucleocytoplasmic transport is bound to illuminate this fundamental biological process in a yet more physiological context. Here, I summarize unresolved questions and evidence and extend basic and critical concepts and challenges of nucleocytoplasmic transport and its role in the pathogenesis of neurodegenerative diseases, such as ALS. These principles will help to appreciate the roles of nucleocytoplasmic transport in the pathogenesis of ALS and other neurodegenerative diseases, and generate a framework for new ideas of the susceptibility of motoneurons, and possibly other neurons, to degeneration by dysregulation of nucleocytoplasmic transport.

Indexed as

Active Transport, Cell NucleusAmyotrophic Lateral SclerosisAnimalsCell NucleusCytoplasmHumansMotor Neuron DiseaseMotor NeuronsNeurodegenerative DiseasesAmyotrophic lateral sclerosis (ALS)Exportin-1/CRM1ImportinKaryopherinMotor neuronsNeurodegenerationNucleocytoplasmic transportNucleoporinRan-binding protein 2 (Ranbp2)Ran GTPase

Identifiers

PMID30742233
PMCPMC6531325

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.