Evidence map›Paper›PMID 16055716›Full record

ArticleMolecular and cellular biology2005

Mice deficient in the fused homolog do not exhibit phenotypes indicative of perturbed hedgehog signaling during embryonic development.

Miao-Hsueh Chen, Nan Gao, Takatoshi Kawakami, Pao-Tien Chuang

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

50 citing papers in PubMed, 114 citations in OpenAlex.

  1. Article
  2. Article
  3. Hedgehog signaling mechanism and role in cancer.Seminars in cancer biology · 2022
    Review
  4. Gli Phosphorylation Code in Hedgehog Signal Transduction.Frontiers in cell and developmental biology · 2022
    Review
  5. Review
  6. Motile cilia genetics and cell biology: big results from little mice.Cellular and molecular life sciences : CMLS · 2021
    Review
  7. Hedgehog Signaling: Implications in Cancers and Viral Infections.International journal of molecular sciences · 2021
    Review
  8. Article
  9. The emerging roles of phosphatases in Hedgehog pathway.Cell communication and signaling : CCS · 2017
    Review
  10. Article
  11. Article
  12. Article
  13. Sonic hedgehog patterning during cerebellar development.Cellular and molecular life sciences : CMLS · 2016
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. G-protein-coupled receptors, Hedgehog signaling and primary cilia.Seminars in cell & developmental biology · 2014
    Review
  20. Article
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 1 institution in 1 country.

Miao-Hsueh ChenCardiovascular Research Institute, University of California, San Francisco, 94143, USA.
Nan Gao
Takatoshi Kawakami
Pao-Tien Chuang
University of California, San Francisco · US

Funding

Hedgehog signal modulation in mammalian developmentR01HL067822 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CHUANG, PAO-TIEN · 2001 to 2011
$3.6M
NHLBI NIH HHS HL67822NHLBI NIH HHS R01 HL067822
6 · The paper itself

Abstract

Hedgehog (Hh) signaling plays a major role in multiple aspects of embryonic development. To understand how a single Hh signal is capable of generating distinct readouts in Hh-responsive cells requires elucidation of the signal transduction cascade at the molecular level. Key components that mediate Hh signal transduction downstream of the receptor include Fused (Fu), Suppressor of fused (Sufu), and Costal-2 (Cos2) or the vertebrate homologs Kif27/Kif7. Studies with both invertebrates and vertebrates have led to a model in which a protein complex composed of Fu, Sufu, and Cos2 controls the processing, activity, and subcellular distribution of the Ci/Gli transcription factors responsible for Hh target gene activation. These converging results obtained with different species reaffirm the prevailing view of pathway conservation during evolution. Genetic studies of Fu, Sufu, and Kif27/Kif7 in mice are required to provide further verification of Hh pathway conservation. To this end, we generated a gene-targeted allele of Fu in mice. Surprisingly, our analysis indicates that Fu-deficient mice do not exhibit any embryonic phenotypes indicative of perturbed Hh signaling. This could be due to either functional redundancy or Hh pathway divergence and clearly indicates greater complexity of Hh signaling in vertebrates.

Indexed as

Gene Expression Regulation, DevelopmentalAllelesAlternative SplicingAnimalsAxin ProteinBlotting, NorthernHedgehog ProteinsIn Situ HybridizationMiceMice, TransgenicModels, GeneticMutationPhenotypeRepressor ProteinsRNA, MessengerSignal TransductionAxin ProteinHedgehog ProteinsRepressor ProteinsRNA, MessengerTrans-Activators

Identifiers

PMID16055716
PMCPMC1190231
OpenAlexW2162146057

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.