Evidence map›Paper›PMID 26023097›Full record

ArticleDevelopment (Cambridge, England)2015

Intraflagellar transport 27 is essential for hedgehog signaling but dispensable for ciliogenesis during hair follicle morphogenesis.

Ning Yang, Li Li, Thibaut Eguether, John P Sundberg, Gregory J Pazour, Jiang Chen

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Development (Cambridge, England), 2015. 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 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Review
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  7. Article
  8. Article
  9. Intraflagellar Transport Proteins as Regulators of Primary Cilia Length.Frontiers in cell and developmental biology · 2021
    Review
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  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 2 countries.

Ning YangDepartments of Pathology and Dermatology, Stony Brook University, Stony Brook, NY 11794, USA.
Li LiDepartment of Dermatology, Peking Union Medical College Hospital, Beijing 100730, China.
Thibaut EguetherProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.
John P SundbergThe Jackson Laboratory, Bar Harbor, ME 04609, USA.
Gregory J PazourProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.
Jiang ChenDepartments of Pathology and Dermatology, Stony Brook University, Stony Brook, NY 11794, USA jiang.chen@stonybrook.edu.
Stony Brook University · USUniversity of Massachusetts Chan Medical School · USJackson Laboratory · USPeking Union Medical College Hospital · CN

Funding

Shared Resource ManagementP30CA034196 · NCI · JACKSON LABORATORY · PI William Carl Skarnes · 1985 to 2026
$61.9M
Intraflagellar Transport Proteins in MiceR01GM060992 · NIGMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI Gregory J Pazour · 2001 to 2026
$10.3M
Planar Cell Polarity Signaling in Hair Follicle FormationR01AR061485 · NIAMS · UNIVERSITY OF COLORADO DENVER · PI CHEN, JIANG · 2011 to 2021
$3.8M
Discovering Novel Gene Networks for Skin DiseasesR21AR063781 · NIAMS · JACKSON LABORATORY · PI SUNDBERG, JOHN PAUL · 2013 to 2014
$422k
NCI NIH HHS P30 CA034196NIAMS NIH HHS AR063781NIAMS NIH HHS R01 AR061485NIAMS NIH HHS R21 AR063781NIGMS NIH HHS GM060992NIGMS NIH HHS R01 GM060992PHS HHS R061485
6 · The paper itself

Abstract

Hair follicle morphogenesis requires precisely controlled reciprocal communications, including hedgehog (Hh) signaling. Activation of the Hh signaling pathway relies on the primary cilium. Disrupting ciliogenesis results in hair follicle morphogenesis defects due to attenuated Hh signaling; however, the loss of cilia makes it impossible to determine whether hair follicle phenotypes in these cilia mutants are caused by the loss of cilia, disruption of Hh signaling, or a combination of these events. In this study, we characterized the function of Ift27, which encodes a subunit of intraflagellar transport (IFT) complex B. Hair follicle morphogenesis of Ift27-null mice was severely impaired, reminiscent of phenotypes observed in cilia and Hh mutants. Furthermore, the Hh signaling pathway was attenuated in Ift27 mutants, which was in association with abnormal ciliary trafficking of SMO and GLI2, and impaired processing of Gli transcription factors; however, formation of the ciliary axoneme was unaffected. The ciliary localization of IFT25 (HSPB11), the binding partner of IFT27, was disrupted in Ift27 mutant cells, and Ift25-null mice displayed hair follicle phenotypes similar to those of Ift27 mutants. These data suggest that Ift27 and Ift25 operate in a genetically and functionally dependent manner during hair follicle morphogenesis. This study suggests that the molecular trafficking machineries underlying ciliogenesis and Hh signaling can be segregated, thereby providing important insights into new avenues of inhibiting Hh signaling, which might be adopted in the development of targeted therapies for Hh-dependent cancers, such as basal cell carcinoma.

Indexed as

AnimalsBiological TransportCell DifferentiationCells, CulturedCiliaHair FollicleHedgehog ProteinsIntracellular Signaling Peptides and ProteinsKeratinocytesKruppel-Like Transcription FactorsMiceMice, KnockoutOrganogenesisProtein Transportrab GTP-Binding ProteinsReceptors, G-Protein-CoupledGli2 protein, mouseHedgehog ProteinsIFT25 protein, mouseIntracellular Signaling Peptides and Proteinsintraflagellar transport 27 protein, mouseKruppel-Like Transcription Factorsrab GTP-Binding ProteinsReceptors, G-Protein-CoupledSmoothened ReceptorSmo protein, mouseZinc Finger Protein Gli2CiliaHair follicleHedgehog signalingIft27Intraflagellar transportMouseSkin

Identifiers

PMID26023097
PMCPMC4483764
OpenAlexW2158680339

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.