Evidence map›Paper›PMID 20940230›Full record

ArticleDevelopment (Cambridge, England)2010

Disabled is a bona fide component of the Abl signaling network.

Jeong K Song, Ramakrishnan Kannan, Gunter Merdes, Jaskirat Singh, Marek Mlodzik, Edward Giniger

Open access · greenAbstract read
In one paragraph

Article in Development (Cambridge, England), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

25 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Dynamic morphogenesis of a pioneer axon inMolecular biology of the cell · 2020
    Article
  9. A new BCR-ABL1Haematologica · 2019
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Notch signaling and neural connectivity.Current opinion in genetics & development · 2012
    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

6 authors at 1 institution in 1 country.

Jeong K SongAxon Guidance and Neural Connectivity Unit, Basic Neuroscience Program, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA.
Ramakrishnan Kannan
Gunter Merdes
Jaskirat Singh
Marek Mlodzik
Edward Giniger
ETH Zurich · CH

Funding

Mechanisms of axon guidance during developmentZIANS003013 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI GINIGER, EDWARD · 2009 to 2025
$17.2M
Roles of Cdk5 in neurodevelopment and neurodegenerationZIANS003106 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI GINIGER, EDWARD · 2009 to 2025
$17.0M
Retinal Patterning During Eye DevelopmentR01EY013256 · NEI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI Marek Mlodzik · 2001 to 2026
$10.0M
Ommatidial rotation and cell motility in the eyeR01EY014597 · NEI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI MLODZIK, MAREK · 2003 to 2011
$3.4M
Mechanisms of axon guidance during developmentZ01NS003013 · NINDS · NEUROLOGICAL DISORDERS AND STROKE · PI GINIGER, EDWARD · 2005 to 2008
$2.0M
Intramural NIH HHS Z01 NS003013NEI NIH HHS EY014597NEI NIH HHS R01 EY013256NEI NIH HHS R01 EY014597NINDS NIH HHS Z01NS003013
6 · The paper itself

Abstract

Abl is an essential regulator of cell migration and morphogenesis in both vertebrates and invertebrates. It has long been speculated that the adaptor protein Disabled (Dab), which is a key regulator of neuronal migration in the vertebrate brain, might be a component of this signaling pathway, but this idea has been controversial. We now demonstrate that null mutations of Drosophila Dab result in phenotypes that mimic Abl mutant phenotypes, both in axon guidance and epithelial morphogenesis. The Dab mutant interacts genetically with mutations in Abl, and with mutations in the Abl accessory factors trio and enabled (ena). Genetic epistasis tests show that Dab functions upstream of Abl and ena, and, consistent with this, we show that Dab is required for the subcellular localization of these two proteins. We therefore infer that Dab is a bona fide component of the core Abl signaling pathway in Drosophila.

Indexed as

AnimalsAnimals, Genetically ModifiedCell MovementDNA-Binding ProteinsDrosophilaDrosophila ProteinsEmbryo, NonmammalianEpistasis, GeneticFemaleGene Regulatory NetworksModels, BiologicalMotor NeuronsMutationNerve Tissue ProteinsProtein-Tyrosine KinasesSignal TransductionAbl protein, Drosophiladab protein, DrosophilaDNA-Binding ProteinsDrosophila ProteinsENA-VASP proteinsNerve Tissue ProteinsProtein-Tyrosine Kinases

Identifiers

PMID20940230
PMCPMC2964101
OpenAlexW2004940993

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.