Evidence map›Paper›PMID 15806168›Full record

ArticleOncogene2005

Gli1 is important for medulloblastoma formation in Ptc1+/- mice.

Hiromichi Kimura, Daniel Stephen, Alexandra Joyner, Tom Curran

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing 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

83 citing papers in PubMed, 145 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Multifaceted Functions of Rab23 on Primary Cilium-Mediated and Hedgehog Signaling-Mediated Cerebellar Granule Cell Proliferation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  13. Review
  14. Article
  15. Cilia, neural development and disease.Seminars in cell & developmental biology · 2021
    Review
  16. Article
  17. The Non-coding Side of Medulloblastoma.Frontiers in cell and developmental biology · 2020
    Review
  18. A novel tumor suppressing gene,Oncology letters · 2020
    Article
  19. Article
  20. Review

23 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

4 authors at 3 institutions in 1 country.

Hiromichi KimuraDepartment of Developmental Neurobiology, St Jude Children's Research Hospital, 332 North Lauderdale, Memphis, TN 38105, USA.
Daniel Stephen
Alexandra Joyner
Tom Curran
St. Jude Children's Research Hospital · USHoward Hughes Medical Institute · USNew York University · US

Funding

The DNA Damage Response and Tumorigenesis in the BrainP01CA096832 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI BAKER, SUZANNE J. · 2003 to 2025
$38.0M
NCI NIH HHS CA096832
6 · The paper itself

Abstract

Germline mutations in the human homolog of the patched1 (PTCH1) are associated with basal cell nevus carcinoma syndrome (BCNS or Gorlin syndrome), which is characterized by developmental anomalies, radiation hypersensitivity and a predisposition to medulloblastomas and skin tumors. Patched1 (Ptc1) functions as a receptor for Sonic hedgehog (Shh) in a wide range of biological processes. Binding of Shh to Ptc1 results in activation of Smoothened (Smo), which in turn stimulates expression of downstream target genes including Ptc1 and Gli1. Gli1 is a member of a family of DNA-binding zinc-finger proteins, including Gli2 and Gli3, that function in transcription control. Here, we report that inactivation of both Gli1 alleles in Ptc1+/- mice significantly reduces spontaneous medulloblastoma formation. Therefore, Gli1 is not only a marker of pathway activation but also plays a functional role in medulloblastoma formation. Interestingly, Gli2 levels were elevated in medulloblastoma cells but not in normal granule neuron precursors during cerebellar development in mice lacking Gli1. In cultured fibroblasts, Gli1 was more potent than Gli2 at inducing cell transformation. These results demonstrate that Gli1 plays a central role in medulloblastoma formation in Ptc1+/- mice and that Gli2 may also contribute to oncogenesis.

Indexed as

AnimalsCerebellar NeoplasmsGenes, ReporterIntracellular Signaling Peptides and ProteinsKruppel-Like Transcription FactorsLuciferasesMedulloblastomaMembrane ProteinsMicePatched-1 ReceptorPatched ReceptorsReceptors, Cell SurfaceTranscription FactorsTranscription, GeneticTumor Cells, CulturedZinc Finger Protein GLI1Gli1 protein, mouseGli2 protein, mouseIntracellular Signaling Peptides and ProteinsKruppel-Like Transcription FactorsLuciferasesMembrane ProteinsPatched-1 ReceptorPatched ReceptorsPTCH1 protein, humanPtch1 protein, mouseReceptors, Cell SurfaceTranscription FactorsZinc Finger Protein GLI1Zinc Finger Protein Gli2

Identifiers

PMID15806168
OpenAlexW2012526118

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.