Evidence map›Paper›PMID 27627892›Full record

ReviewRNA biology2017

Cajal bodies in neurons.

Miguel Lafarga, Olga Tapia, Ana M Romero, Maria T Berciano

Open access · bronzeAbstract readReview
In one paragraph

Review in RNA biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.0field-weighted citation impact, top 14% of its field
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

32 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Coilin and Cajal bodies.Nucleus (Austin, Tex.) · 2023
    Review
  8. Article
  9. Article
  10. The Role of WRAP53 in Cell Homeostasis and Carcinogenesis Onset.Current issues in molecular biology · 2022
    Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 1 country.

Miguel Lafargaa Departamento de Anatomía y Biología Celular and "Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED)" , Universidad de Cantabria-IDIVAL , Santander , Spain.
Olga Tapiaa Departamento de Anatomía y Biología Celular and "Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED)" , Universidad de Cantabria-IDIVAL , Santander , Spain.
Ana M Romeroa Departamento de Anatomía y Biología Celular and "Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED)" , Universidad de Cantabria-IDIVAL , Santander , Spain.
Maria T Bercianoa Departamento de Anatomía y Biología Celular and "Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED)" , Universidad de Cantabria-IDIVAL , Santander , Spain.
Instituto de Investigación Marqués de Valdecilla · ESBiomedical Research Networking Center on Neurodegenerative Diseases · ESUniversidad de Cantabria · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cajal is commonly regarded as the father of modern neuroscience in recognition of his fundamental work on the structure of the nervous system. But Cajal also made seminal contributions to the knowledge of nuclear structure in the early 1900s, including the discovery of the "accessory body" later renamed "Cajal body" (CB). This important nuclear structure has emerged as a center for the assembly of ribonucleoproteins (RNPs) required for splicing, ribosome biogenesis and telomere maintenance. The modern era of CB research started in the 1990s with the discovery of coilin, now known as a scaffold protein of CBs, and specific probes for small nuclear RNAs (snRNAs). In this review, we summarize what we have learned in the recent decades concerning CBs in post-mitotic neurons, thereby ruling out dynamic changes in CB functions during the cell cycle. We show that CBs are particularly prominent in neurons, where they frequently associate with the nucleolus. Neuronal CBs are transcription-dependent nuclear organelles. Indeed, their number dynamically accommodates to support the high neuronal demand for splicing and ribosome biogenesis required for sustaining metabolic and bioelectrical activity. Mature neurons have canonical CBs enriched in coilin, survival motor neuron protein and snRNPs. Disruption and loss of neuronal CBs associate with severe neuronal dysfunctions in several neurological disorders such as motor neuron diseases. In particular, CB depletion in motor neurons seems to reflect a perturbation of transcription and splicing in spinal muscular atrophy, the most common genetic cause of infant mortality.

Indexed as

AnimalsCell NucleolusCoiled BodiesDisease SusceptibilityHumansNervous System DiseasesNeuronsNuclear ProteinsProtein TransportRibonucleoproteins, Small NuclearRNA, Small NuclearRNA SplicingNuclear Proteinsp80-coilinRibonucleoproteins, Small NuclearRNA, Small NuclearAmyotrophic lateral sclerosisCajal bodycoilinneurodegenerationneuronsnucleoluspre-mRNA splicingsnRNPspinal muscular atrophysurvival motor neuron

Identifiers

PMID27627892
PMCPMC5519235
OpenAlexW2519157528

What OpenQuestion holds

Textmetadata
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.