Evidence map›Paper›PMID 37291945›Full record

ArticleEMBO reports2023

LTK and ALK promote neuronal polarity and cortical migration by inhibiting IGF1R activity.

Tania Christova, Stephanie Ky Ho, Ying Liu, Mandeep Gill, Liliana Attisano

Open access · bronzeAbstract read
In one paragraph

Article in EMBO reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

11 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. AlkCell communication and signaling : CCS · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Therapeutic advances of targeting receptor tyrosine kinases in cancer.Signal transduction and targeted therapy · 2024
    Review
  9. Article
  10. Article
  11. 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 1 institution in 1 country.

Tania Christova *Department of Biochemistry, Donnelly Centre, University of Toronto, Toronto, ON, Canada.
Stephanie Ky Ho *Department of Biochemistry, Donnelly Centre, University of Toronto, Toronto, ON, Canada.
Ying LiuDepartment of Biochemistry, Donnelly Centre, University of Toronto, Toronto, ON, Canada.
Mandeep GillDepartment of Biochemistry, Donnelly Centre, University of Toronto, Toronto, ON, Canada.
Liliana AttisanoDepartment of Biochemistry, Donnelly Centre, University of Toronto, Toronto, ON, Canada.ORCID 0000-0003-4824-2642
University of Toronto · CA

Funding

Canadian Institute for Health Research FDN148455
6 · The paper itself

Abstract

The establishment of axon-dendrite polarity is fundamental for radial migration of neurons, cortical patterning, and formation of neuronal circuits. Here, we show that the receptor tyrosine kinases, Ltk and Alk, are required for proper neuronal polarization. In isolated primary mouse embryonic neurons, the loss of Ltk and/or Alk causes a multiple axon phenotype. In mouse embryos and newborn pups, the absence of Ltk and Alk delays neuronal migration and subsequent cortical patterning. In adult cortices, neurons with aberrant neuronal projections are evident and axon tracts in the corpus callosum are disrupted. Mechanistically, we show that the loss of Alk and Ltk increases the cell-surface expression and activity of the insulin-like growth factor 1 receptor (Igf-1r), which activates downstream PI3 kinase signaling to drive the excess axon phenotype. Our data reveal Ltk and Alk as new regulators of neuronal polarity and migration whose disruption results in behavioral abnormalities.

Indexed as

NeuronsReceptor Protein-Tyrosine KinasesAnaplastic Lymphoma KinaseAnimalsAxonsCell PolarityMiceNeurogenesisReceptor, IGF Type 1Signal TransductionAlk protein, mouseAnaplastic Lymphoma KinaseIgf1r protein, mouseLtk protein, mouseReceptor, IGF Type 1Receptor Protein-Tyrosine KinasesALKcortical migrationIGF-1RLTKneuronal polarity

Identifiers

PMID37291945
PMCPMC10328079
OpenAlexW4379966429

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.