Evidence map›Paper›PMID 25848697›Full record

ArticleDevelopmental biology2015

Distinct structural requirements for CDON and BOC in the promotion of Hedgehog signaling.

Jane Y Song, Alexander M Holtz, Justine M Pinskey, Benjamin L Allen

Abstract readComparative Study
In one paragraph

Article in Developmental biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Article
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  11. Review
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  14. Mechanism of inhibition of the tumor suppressor Patched by Sonic Hedgehog.Proceedings of the National Academy of Sciences of the United States of America · 2016
    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.

Jane Y SongDepartment of Cell and Developmental Biology, University of Michigan, Ann Arbor, MI 48109, USA.
Alexander M HoltzDepartment of Cell and Developmental Biology, University of Michigan, Ann Arbor, MI 48109, USA; Medical Scientist Training Program, University of Michigan, Ann Arbor, MI 48109, USA; Cellular and Molecular Biology Program, University of Michigan, Ann Arbor, MI 48109, USA.
Justine M PinskeyDepartment of Cell and Developmental Biology, University of Michigan, Ann Arbor, MI 48109, USA.
Benjamin L AllenDepartment of Cell and Developmental Biology, University of Michigan, Ann Arbor, MI 48109, USA. Electronic address: benallen@umich.edu.

Funding

MICHIGAN MEDICAL SCIENTIST TRAINING PROGRAMT32GM007863 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI COLLINS, KATHLEEN L. · 1985 to 2024
$38.3M
Tissue Engineering and RegenerationT32DE007057 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DAVID H. KOHN · 1985 to 2026
$17.3M
CELLULAR AND MOLECULAR BIOLOGY AT MICHIGANT32GM007315 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PUTHENVEEDU, MANOJKUMAR A · 1985 to 2021
$12.8M
TRAINING PROGRAM IN ORGANOGENESIST32HD007505 · NICHD · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PASCA DI MAGLIANO, MARINA, SPENCE, JASON · 1997 to 2021
$6.9M
Hedgehog signaling in maintaining taste organ structure and function: basic and clinical studiesR01DC014428 · NIDCD · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ALLEN, BENJAMIN, BRADLEY, ROBERT M · 2015 to 2019
$3.3M
Novel Hedgehog Receptors As Therapeutic Targets In Pancreatic CancerR21CA167122 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ALLEN, BENJAMIN, PASCA DI MAGLIANO, MARINA · 2012 to 2013
$364k
PTCH2-Mediated Antagonism of Hedgehog Signaling During Vertebrate Neural PatterniF31NS081806 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HOLTZ, ALEXANDER MATTHEW · 2013 to 2013
$33k
NCI NIH HHS R21 CA167122NCI NIH HHS R21CA167122NICHD NIH HHS T32 HD007505NIDCD NIH HHS R01 DC014428NIDCD NIH HHS R01DC014428NIDCR NIH HHS T32 DE007057NIGMS NIH HHS T32 GM007315NIGMS NIH HHS T32 GM007863NINDS NIH HHS F31 NS081806NINDS NIH HHS F31NS081806
6 · The paper itself

Abstract

Proper levels of Hedgehog (HH) signaling are essential during embryonic development and adult tissue homeostasis. A central mechanism to control HH pathway activity is through the regulation of secreted HH ligands at the plasma membrane. Recent studies have revealed a collective requirement for the cell surface co-receptors GAS1, CDON and BOC in HH signal transduction. Despite their requirement in HH pathway function, the mechanisms by which these proteins act to promote HH signaling remain poorly understood. Here we focus on the function of the two structurally related co-receptors, CDON and BOC. We utilized an in vivo gain-of-function approach in the developing chicken spinal cord to dissect the structural requirements for CDON and BOC function in HH signal transduction. Notably, we find that although CDON and BOC display functional redundancy during HH-dependent ventral neural patterning, these molecules utilize distinct molecular mechanisms to execute their HH-promoting effects. Specifically, we define distinct membrane attachment requirements for CDON and BOC function in HH signal transduction. Further, we identify novel and separate extracellular motifs in CDON and BOC that are required to promote HH signaling. Together, these data suggest that HH co-receptors employ distinct mechanisms to mediate HH pathway activity.

Indexed as

AnimalsBlotting, WesternCell Adhesion MoleculesCell MembraneChick EmbryoChlorocebus aethiopsCOS CellsElectrophoresis, Polyacrylamide GelElectroporationFluorescent Antibody TechniqueHedgehog ProteinsImage Processing, Computer-AssistedImmunoprecipitationModels, MolecularProtein Structure, TertiaryReceptors, Cell SurfaceCell Adhesion MoleculesHedgehog ProteinsReceptors, Cell SurfaceBOCCDONCo-receptorHedgehogNeural patterning

Identifiers

PMID25848697
PMCPMC4450140

What OpenQuestion holds

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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.