Evidence map›Paper›PMID 26271100›Full record

ArticlePloS one2015

A Comparison of Ci/Gli Activity as Regulated by Sufu in Drosophila and Mammalian Hedgehog Response.

Sekyung Oh, Masaki Kato, Chi Zhang, Yurong Guo, Philip A Beachy

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Cellular and molecular mechanisms of Hedgehog signalling.Nature reviews. Molecular cell biology · 2023
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. 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

5 authors at 2 institutions in 1 country.

Sekyung OhDepartment of Developmental Biology, Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, California, United States of America; Department of Molecular Biology and Genetics, Howard Hughes Medical Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
Masaki KatoDepartment of Developmental Biology, Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, California, United States of America; Department of Molecular Biology and Genetics, Howard Hughes Medical Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
Chi ZhangDepartment of Molecular Biology and Genetics, Howard Hughes Medical Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
Yurong GuoDivision of Pulmonary and Critical Care Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
Philip A BeachyDepartment of Developmental Biology, Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, California, United States of America; Department of Molecular Biology and Genetics, Howard Hughes Medical Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America; Department of Biochemistry, Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, California, United States of America.
Johns Hopkins University · USStanford University · US

Funding

TRANSPOSITION OF TN7P01CA016519 · NCI · JOHNS HOPKINS UNIVERSITY · PI BOEKE, JEF D · 1985 to 2010
$21.4M
Molecular mechanisms of Hedgehog receptor functionR01GM102498 · NIGMS · STANFORD UNIVERSITY · PI PHILIP A BEACHY · 2012 to 2026
$4.5M
Howard Hughes Medical InstituteNCI NIH HHS P01 CA016519NIGMS NIH HHS 5R01GM102498NIGMS NIH HHS R01 GM102498
6 · The paper itself

Abstract

Suppressor of fused (Su(fu)/Sufu), one of the most conserved components of the Hedgehog (Hh) signaling pathway, binds Ci/Gli transcription factors and impedes activation of target gene expression. In Drosophila, the Su(fu) mutation has a minimal phenotype, and we show here that Ci transcriptional activity in large part is regulated independently of Su(fu) by other pathway components. Mutant mice lacking Sufu in contrast show excessive pathway activity and die as embryos with patterning defects. Here we show that in cultured cells Hh stimulation can augment transcriptional activity of a Gli2 variant lacking Sufu interaction and, surprisingly, that regulation of Hh pathway targets is nearly normal in the neural tube of Sufu-/- mutant embryos that also lack Gli1 function. Some degree of Hh-induced transcriptional activation of Ci/Gli thus can occur independently of Sufu in both flies and mammals. We further note that Sufu loss can also reduce Hh induction of high-threshold neural tube fates, such as floor plate, suggesting a possible positive pathway role for Sufu.

Indexed as

AnimalsDNA-Binding ProteinsDrosophilaDrosophila ProteinsHedgehog ProteinsKinesinsMiceMice, Mutant StrainsOncogene ProteinsProtein Serine-Threonine KinasesRepressor ProteinsSignal TransductionTrans-ActivatorsTranscription FactorsZinc Finger Protein GLI1ci protein, Drosophilacos protein, DrosophilaDNA-Binding ProteinsDrosophila Proteinsfu protein, DrosophilaHedgehog ProteinsKinesinsOncogene ProteinsProtein Serine-Threonine KinasesRepressor ProteinsSu(fu) protein, DrosophilaTrans-ActivatorsTranscription FactorsZinc Finger Protein GLI1

Identifiers

PMID26271100
PMCPMC4536226
OpenAlexW1751133475

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.