Evidence map›Paper›PMID 29596897›Full record

ReviewMolecular and cellular neurosciences2018

Mechanisms of neurotrophin trafficking via Trk receptors.

Emily Scott-Solomon, Rejji Kuruvilla

Abstract readReview
In one paragraph

Review in Molecular and cellular neurosciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
8.2field-weighted citation impact, top 1% 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

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 116 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Junctions in Jeopardy: the neuromuscular junction is a selective pathological target in Charcot-Marie-Tooth disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Review
  6. Review
  7. Article
  8. International journal of molecular sciences · 2026
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. PLC-γ-CaFrontiers in molecular neuroscience · 2024
    Article
  17. Article
  18. Article
  19. Review
  20. Article

2 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Emily Scott-SolomonDepartment of Biology, Johns Hopkins University, 3400 N. Charles St, 227 Mudd Hall, Baltimore, MD 21218, USA.
Rejji KuruvillaDepartment of Biology, Johns Hopkins University, 3400 N. Charles St, 227 Mudd Hall, Baltimore, MD 21218, USA. Electronic address: rkuruvilla@jhu.edu.
Johns Hopkins University · US

Funding

CELLULAR AND MOLECULAR BIOLOGYT32GM007231 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI VAN DOREN, MARK B · 1985 to 2020
$18.4M
Neurotrophin mechanisms in neural development and diseaseR01NS073751 · NINDS · JOHNS HOPKINS UNIVERSITY · PI KURUVILLA, REJJI · 2011 to 2015
$1.7M
Neurotrophins as new regulators of islet biologyR01DK108267 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI KURUVILLA, REJJI · 2016 to 2019
$1.4M
NIDDK NIH HHS R01 DK108267NIGMS NIH HHS T32 GM007231NINDS NIH HHS R01 NS073751
6 · The paper itself

Abstract

In neurons, long-distance communication between axon terminals and cell bodies is a critical determinant in establishing and maintaining neural circuits. Neurotrophins are soluble factors secreted by post-synaptic target tissues that retrogradely control axon and dendrite growth, survival, and synaptogenesis of innervating neurons. Neurotrophins bind Trk receptor tyrosine kinases in axon terminals to promote endocytosis of ligand-bound phosphorylated receptors into signaling endosomes. Trk-harboring endosomes function locally in axons to acutely promote growth events, and can also be retrogradely transported long-distances to remote cell bodies and dendrites to stimulate cytoplasmic and transcriptional signaling necessary for neuron survival, morphogenesis, and maturation. Neuronal responsiveness to target-derived neurotrophins also requires the precise axonal targeting of newly synthesized Trk receptors. Recent studies suggest that anterograde delivery of Trk receptors is regulated by retrograde neurotrophin signaling. In this review, we summarize current knowledge on the functions and mechanisms of retrograde trafficking of Trk signaling endosomes, and highlight recent discoveries on the forward trafficking of nascent receptors.

Indexed as

AnimalsAxonsEndosomesHumansNerve Growth FactorsProtein TransportReceptor Tyrosine Kinase-like Orphan ReceptorsSignal TransductionSynapsesNerve Growth FactorsReceptor Tyrosine Kinase-like Orphan Receptors

Identifiers

PMID29596897
PMCPMC6128733
OpenAlexW2795126113

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.