Evidence map›Paper›PMID 15104233›Full record

ReviewBiochemical pharmacology2004

Regulation of Hedgehog signaling: a complex story.

Stacey K Ogden, Manuel Ascano, Melanie A Stegman, David J Robbins

Abstract readReview
In one paragraph

Review in Biochemical pharmacology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.4field-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

36 citing papers in PubMed, 111 citations in OpenAlex.

  1. Article
  2. Tai/NCOA2 suppresses the Hedgehog pathway by directly targeting the transcription factor Ci/GLI.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. GLI3: a mediator of genetic diseases, development and cancer.Cell communication and signaling : CCS · 2020
    Review
  11. Article
  12. Article
  13. Article
  14. Optimized strategy for in vivo Cas9-activation inProceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Genetic interaction screens identify a role for hedgehog signaling in Drosophila border cell migration.Developmental dynamics : an official publication of the American Association of Anatomists · 2013
    Article
  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 2 institutions in 1 country.

Stacey K OgdenDepartment of Pharmacology and Toxicology, Dartmouth Medical School, 7650 Remsen Hall, Hanover, NH 03755-3835, USA.
Manuel Ascano
Melanie A Stegman
David J Robbins
Dartmouth College · USUniversity of Cincinnati Medical Center · US

Funding

RECONSTITUTION OF HEDGEHOG SIGNALING COMPLEXR01CA082628 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI ROBBINS, DAVID J · 1999 to 2014
$4.1M
NCI NIH HHS CA82628NCI NIH HHS R01 CA082628
6 · The paper itself

Abstract

The Hedgehog (Hh) signal transduction pathway plays critical instructional roles during development. Activating mutations in human Hh signaling components predispose to a variety of tumor types, and have been observed in sporadic tumors occurring in a wide range of organs. Multiple insights into the regulation of Hh signaling have been achieved through studies using Drosophila melanogaster as a model organism. In Drosophila, regulation of the transcription factor Cubitus interruptus (Ci) is the ultimate target of the Hh pathway. Ci is regulated through communication of the membrane proteins Patched (Ptc) and Smoothened (Smo) to the intracellular Hedgehog Signaling Complex (HSC) in response to a graded concentration of Hh ligand. The HSC consists of the Kinesin Related Protein, Costal2 (Cos2), the serine-threonine protein kinase. Fused (Fu) and Ci. In the absence of Hh stimulation, the HSC is involved in processing of Ci to a truncated repressor protein. In response to Hh binding to Ptc, processing of Ci is blocked to allow for accumulation of full-length Ci activator protein(s). Differential concentrations of Hh ligand stimulate production of Ci transcriptional activators of varying strength, which facilitate activation of distinct subsets of target genes. The mechanism(s) by which Ptc and Smo communicate with the HSC in response to differential ligand concentrations to regulate Ci function are not yet fully elucidated. Here, we review what is known about regulation of individual Hh signaling components, concentrating on the mechanisms by which the Hh signal is propagated through Smo to the HSC.

Indexed as

AnimalsDNA-Binding ProteinsDrosophila melanogasterDrosophila ProteinsHedgehog ProteinsKinesinsMammalsReceptors, G-Protein-CoupledRepressor ProteinsSignal TransductionSmoothened ReceptorTrans-ActivatorsTranscription Factorsci protein, Drosophilacos protein, DrosophilaDNA-Binding ProteinsDrosophila ProteinsHedgehog Proteinshh protein, DrosophilaKinesinsReceptors, G-Protein-CoupledRepressor ProteinsSmoothened Receptorsmo protein, DrosophilaSu(fu) protein, DrosophilaSUFU protein, humanTrans-ActivatorsTranscription Factors

Identifiers

PMID15104233
PMCPMC3659400
OpenAlexW2095217788

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.