Evidence map›Paper›PMID 22446182›Full record

ArticleThe Journal of clinical investigation2012

A "so cilia" network: cilia proteins start "social" networking.

Frédéric Saudou

Open access · bronzeAbstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 31% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Digenic inheritance in medical genetics.Journal of medical genetics · 2013
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Frédéric SaudouInstitut Curie, CNRS UMR3306, and INSERM U1005, Orsay, France. Frederic.Saudou@curie.fr
Inserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cilia are unique cellular organelles found in nearly all cell types. In recent years, the importance of these organelles has been highlighted by the discovery that mutations in genes encoding proteins related to cilia biogenesis and function cause a class of complex syndromes termed ciliopathies. Emerging evidence suggests interactions among the various ciliopathy-associated proteins, but the precise mechanisms by which these interactions generate functional networks have remained elusive. In this issue of the JCI, Rachel and colleagues have now clearly linked two ciliopathy-associated proteins (CEP290 and MKKS). Surprisingly, the effects of a hypomorphic disease-causing Cep290 allele were rescued by loss of MKKS function, suggesting that it might be possible to treat some ciliopathies by fine-tuning interactions within the expanding ciliary network.

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsAntigens, NeoplasmBardet-Biedl SyndromeCell Cycle ProteinsCiliaCytoskeletal ProteinsGroup II ChaperoninsHumansLeber Congenital AmaurosisNeoplasm ProteinsNuclear ProteinsSensation DisordersAntigens, NeoplasmCell Cycle ProteinsCep290 protein, humanCep290 protein, mouseCytoskeletal ProteinsGroup II ChaperoninsMKKS protein, humanMkks protein, mouseNeoplasm ProteinsNuclear Proteins

Identifiers

PMID22446182
PMCPMC3314480
OpenAlexW2092982793

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.