Evidence map›Paper›PMID 23982746›Full record

ReviewMolecular neurobiology2014

Receptor tyrosine kinase (RTK) signalling in the control of neural stem and progenitor cell (NSPC) development.

Alexander Annenkov

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

15 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Predicting Novel Drug Candidates for Pancreatic Neuroendocrine Tumors via Gene Signature Comparison and Connectivity Mapping.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2022
    Article
  5. Article
  6. Article
  7. Genomic Survey of Tyrosine Kinases Repertoire inEvolutionary bioinformatics online · 2020
    Article
  8. TRPM7, Magnesium, and Signaling.International journal of molecular sciences · 2019
    Review
  9. [Progress on neurogenesis mechanisms of endogenous adult neural stem cells].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2018
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. 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

1 author at 1 institution in 1 country.

Alexander AnnenkovBone and Joint Research Unit, William Harvey Research Institute, Bart's and The London School of Medicine, Queen Mary University of London, Charterhouse Square, London, EC1M 6BQ, UK, a.annenkov@qmul.ac.uk.
Queen Mary University of London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Important developmental responses are elicited in neural stem and progenitor cells (NSPC) by activation of the receptor tyrosine kinases (RTK), including the fibroblast growth factor receptors, epidermal growth factor receptor, platelet-derived growth factor receptors and insulin-like growth factor receptor (IGF1R). Signalling through these RTK is necessary and sufficient for driving a number of developmental processes in the central nervous system. Within each of the four RTK families discussed here, receptors are activated by sets of ligands that do not cross-activate receptors of the other three families, and therefore, their activation can be independently regulated by ligand availability. These RTK pathways converge on a conserved core of signalling molecules, but differences between the receptors in utilisation of signalling molecules and molecular adaptors for intracellular signal propagation become increasingly apparent. Intracellular inhibitors of RTK signalling are widely involved in the regulation of developmental signalling in NSPC and often determine developmental outcomes of RTK activation. In addition, cellular responses of NSPC to the activation of a given RTK may be significantly modulated by signal strength. Cellular propensity to respond also plays a role in developmental outcomes of RTK signalling. In combination, these mechanisms regulate the balance between NSPC maintenance and differentiation during development and in adulthood. Attribution of particular developmental responses of NSPC to specific pathways of RTK signalling becomes increasingly elucidated. Co-activation of several RTK in developing NSPC is common, and analysis of co-operation between their signalling pathways may advance knowledge of RTK role in NSPC development.

Indexed as

AnimalsBrainCell DifferentiationCell MovementHumansNeural Stem CellsReceptor Protein-Tyrosine KinasesSignal TransductionStem CellsReceptor Protein-Tyrosine Kinases

Identifiers

PMID23982746
OpenAlexW1977167934

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.