Evidence map›Paper›PMID 22840514›Full record

ArticleCurrent biology : CB2012

Supernumerary centrosomes nucleate extra cilia and compromise primary cilium signaling.

Moe R Mahjoub, Tim Stearns

Open access · bronzeAbstract read
In one paragraph

Article in Current biology : CB, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
10.5field-weighted citation impact, top 1% 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

72 citing papers in PubMed, 117 citations in OpenAlex.

  1. The roles of centrosome amplification in diabetes-associated diseases.Frontiers in cell and developmental biology · 2026
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  12. Cholesterol and Phosphoinositides in Cilia Biology.Advances in experimental medicine and biology · 2023
    Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Roles for ELMOD2 and Rootletin in ciliogenesis.Molecular biology of the cell · 2021
    Article
  20. Article

12 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

Moe R MahjoubDepartment of Biology, Stanford University, Stanford, CA 94305, USA.
Tim Stearns
Stanford Medicine · USStanford University · US

Funding

GAMMA TUBULIN AND CENTROSOME STRUCTURE AND FUNCTIONR01GM052022 · NIGMS · STANFORD UNIVERSITY · PI STEARNS, TIM · 1995 to 2017
$6.5M
NIGMS NIH HHS GM52022NIGMS NIH HHS R01 GM052022
6 · The paper itself

Abstract

The primary cilium is a nexus of cell signaling, and ciliary dysfunction is associated with polycystic kidney disease, retinal degeneration, polydactyly, neural tube defects, and obesity (ciliopathies). Signaling molecules for cilium-associated pathways are concentrated in the cilium, and this is essential for efficient signaling. Cilia are nucleated from centrioles, and aberrant centriole numbers are seen in many cancers and in some ciliopathies. We tested the effect of supernumerary centrioles on cilium function and found that cells with extra centrioles often formed more than one cilium, had reduced ciliary concentration of Smoothened in response to Sonic hedgehog stimulation, and reduced Shh pathway transcriptional activation. This ciliary dilution phenotype was also observed with the serotonin receptor Htr6, fibrocystin PKHD1, and Arl13b. The presence of extra centrioles and cilia disrupted epithelial organization in 3D spheroid culture. Cells mutant for the tuberous sclerosis gene Tsc2 also had extra cilia and diluted ciliary protein. In most cells, extra cilia were clustered and shared the same ciliary pocket, suggesting that the ciliary pocket is the rate-limiting structure for trafficking of ciliary proteins. Thus, extra centrioles and cilia disrupt signaling and may contribute to disease phenotypes.

Indexed as

Signal TransductionAnimalsCentrosomeCiliaHedgehog ProteinsMiceNIH 3T3 CellsPhenotypeReceptors, G-Protein-CoupledSmoothened ReceptorTuberous Sclerosis Complex 2 ProteinTumor Suppressor ProteinsHedgehog ProteinsReceptors, G-Protein-CoupledShh protein, mouseSmoothened ReceptorSmo protein, mouseTsc2 protein, mouseTuberous Sclerosis Complex 2 ProteinTumor Suppressor Proteins

Identifiers

PMID22840514
PMCPMC4094149
OpenAlexW2091287948

What OpenQuestion holds

Textmetadata
LicenceTDM
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.