Evidence map›Paper›PMID 33625872›Full record

ArticleMolecular biology of the cell2021

Rpgrip1l controls ciliary gating by ensuring the proper amount of Cep290 at the vertebrate transition zone.

Antonia Wiegering, Renate Dildrop, Christine Vesque, Hemant Khanna, Sylvie Schneider-Maunoury, Christoph Gerhardt

Open access · bronzeAbstract read
In one paragraph

Article in Molecular biology of the cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Eupatilin improves cilia defects in human CEP290 ciliopathy models.bioRxiv : the preprint server for biology · 2023
    Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  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

6 authors at 3 institutions in 3 countries.

Antonia WiegeringInstitute for Animal Developmental and Molecular Biology, Heinrich Heine University, 40225 Düsseldorf, Germany.
Renate DildropInstitute for Animal Developmental and Molecular Biology, Heinrich Heine University, 40225 Düsseldorf, Germany.
Christine VesqueSorbonne Université, CNRS UMR7622, INSERM U1156, Institut de Biologie Paris Seine (IBPS) - Developmental Biology Unit, 75005 Paris, France.
Hemant KhannaDepartment of Ophthalmology and Neurobiology, University of Massachusetts Medical School, Worcester, MA 01605.
Sylvie Schneider-MaunourySorbonne Université, CNRS UMR7622, INSERM U1156, Institut de Biologie Paris Seine (IBPS) - Developmental Biology Unit, 75005 Paris, France.
Christoph GerhardtInstitute for Animal Developmental and Molecular Biology, Heinrich Heine University, 40225 Düsseldorf, Germany.
Centre National de la Recherche Scientifique · FRHeinrich Heine University Düsseldorf · DEUniversity of Massachusetts Chan Medical School · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A range of severe human diseases called ciliopathies is caused by the dysfunction of primary cilia. Primary cilia are cytoplasmic protrusions consisting of the basal body (BB), the axoneme, and the transition zone (TZ). The BB is a modified mother centriole from which the axoneme, the microtubule-based ciliary scaffold, is formed. At the proximal end of the axoneme, the TZ functions as the ciliary gate governing ciliary protein entry and exit. Since ciliopathies often develop due to mutations in genes encoding proteins that localize to the TZ, the understanding of the mechanisms underlying TZ function is of eminent importance. Here, we show that the ciliopathy protein Rpgrip1l governs ciliary gating by ensuring the proper amount of Cep290 at the vertebrate TZ. Further, we identified the flavonoid eupatilin as a potential agent to tackle ciliopathies caused by mutations in

Indexed as

Adaptor Proteins, Signal TransducingAnimalsAntigens, NeoplasmAxonemeBasal BodiesCell Cycle ProteinsCentriolesCiliaCiliopathiesCytoskeletal ProteinsHEK293 CellsHumansMiceMutationNIH 3T3 CellsSignal TransductionAdaptor Proteins, Signal TransducingAntigens, NeoplasmCell Cycle ProteinsCep290 protein, humanCep290 protein, mouseCytoskeletal ProteinsFtm protein, mouseRPGRIP1L protein, human

Identifiers

PMID33625872
PMCPMC8108517
OpenAlexW3133430347

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.