Evidence map›Paper›PMID 39576500›Full record

ReviewAnatomical science international2025

Regulatory mechanisms governing GLI proteins in hedgehog signaling.

Saishu Yoshida, Kiyotsugu Yoshida

Abstract readReview
PubMed Publisher
In one paragraph

Review in Anatomical science international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Bioinformatics analysis identifiesTranslational cancer research · 2025
    Article
  2. Article
  3. Article
  4. Article
  5. Review
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.

Saishu YoshidaDepartment of Biomolecular Science, Faculty of Science, Toho University, Chiba, 274-8510, Japan. saishu.yoshida@sci.toho-u.ac.jp.ORCID http://orcid.org/0000-0002-2574-6410
Kiyotsugu YoshidaDepartment of Biochemistry, The Jikei University School of Medicine, Tokyo, 105-8461, Japan.

Funding

Japan Society for the Promotion of Science 21K06192Japan Society for the Promotion of Science 23K18244Japan Society for the Promotion of Science 24K10341
6 · The paper itself

Abstract

The Hedgehog (Hh) signaling pathway is critical for regulating cell growth, survival, fate determination, and the overall patterning of both vertebrate and invertebrate body plans. Aberrations in Hh signaling are associated with congenital abnormalities and tumorigenesis. In vertebrates, Hh signaling depends uniquely on primary cilia, microtubule-based organelles that extend from the cell surface. Over the last 2 decades, studies have demonstrated that key molecules regulating Hh signaling dynamically accumulate in primary cilia via intraflagellar transport systems. Moreover, through the primary cilia, extracellular signals are converted to stabilize GLI2 and GLI3 that are transcription factors that play a central role in regulating Hh signaling at the post-translational modification level. Recent in vivo and anatomical studies have uncovered crucial molecules that facilitate the conversion of extracellular signals into the intracellular stabilization of GLI2/GLI3 via primary cilia, emphasizing their essential roles in tissue development and tumorigenesis. This review explores the regulatory mechanisms of GLI2/GLI3 with a focus on mammalian tissue development.

Indexed as

Hedgehog ProteinsSignal TransductionZinc Finger Protein Gli2Zinc Finger Protein Gli3AnimalsCiliaHumansNuclear ProteinsGLI2 protein, humanHedgehog ProteinsNuclear ProteinsZinc Finger Protein Gli2Zinc Finger Protein Gli3DevelopmentGLIHedgehog signalingPrimary ciliaTumorigenesis

Identifiers

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.