Evidence map›Paper›PMID 11007890›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000

NGF signals through TrkA to increase clathrin at the plasma membrane and enhance clathrin-mediated membrane trafficking.

E C Beattie, C L Howe, A Wilde, F M Brodsky, W C Mobley

Open access · greenAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

48 citing papers in PubMed, 133 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. NGF Signaling in Endosomes.Advances in experimental medicine and biology · 2021
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. TrkB neurotrophic activities are blocked by α-synuclein, triggering dopaminergic cell death in Parkinson's disease.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Biogenesis and function of the NGF/TrkA signaling endosome.International review of cell and molecular biology · 2015
    Review
  19. Review
  20. 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 4 institutions in 3 countries.

E C BeattieDepartment of Physiology, University of California at San Francisco, San Francisco, California 94143, USA.
C L Howe
A Wilde
F M Brodsky
W C Mobley
San Francisco Foundation · USCzech Academy of Sciences, Institute of Physiology · CZSociety for Neuroscience · USStanford University · US

Funding

THE MOLECULAR MECHANISM OF CLATHRIN ASSEMBLYR01GM038093 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BRODSKY, FRANCES M. · 1988 to 2014
$5.0M
ADA3: a novel target for HPV16 E6 oncoproteinR01CA094143 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BAND, VIMLA · 2002 to 2006
$1.7M
NERVE GROWTH FACTOR--TROPHIC EFFECTS ON CNS NEURONSR01NS024054 · NINDS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI MOBLEY, WILLIAM C · 1986 to 2008
$1.6M
NCI NIH HHS R01 CA094143NIGMS NIH HHS GM38093NIGMS NIH HHS R01 GM038093NINDS NIH HHS NS24054NINDS NIH HHS R01 NS024054
6 · The paper itself

Abstract

Neurotrophin (NT) signals may be moved from axon terminals to neuron cell bodies via signaling endosomes-organelles in which NTs continue to be bound to their activated receptors. Suggesting that clathrin-coated membranes serve as one source of signaling endosomes, in earlier studies we showed that nerve growth factor (NGF) treatment increased clathrin at the plasma membrane and resulted in colocalization of clathrin with TrkA, the receptor tyrosine kinase for NGF. Strikingly, however, we also noted that most clathrin puncta at the surface of NGF-treated cells did not colocalize with TrkA, raising the possibility that NGF induces a general increase in clathrin-coated membrane formation. To explore this possibility further, we examined the distribution of clathrin in NGF- and BDNF-treated cells. NGF signaling in PC12 cells robustly redistributed the adaptor protein AP2 and the clathrin heavy chain (CHC) to surface membranes. Using confocal and epifluorescence microscopy, as well as biochemical assays, we showed the redistribution of clathrin to be attributable to the activation of TrkA. Significantly, NGF signaled through TrkA to induce an increase in clathrin-mediated membrane trafficking, as revealed in the increased endocytosis of transferrin. In that BDNF treatment increased AP2 and clathrin at the surface membranes of hippocampal neurons, these findings may represent a physiologically significant response to NTs. We conclude that NT signaling increases clathrin-coated membrane formation and clathrin-mediated membrane trafficking and speculate that this effect contributes to their trophic actions via the increased internalization of receptors and other proteins that are present in clathrin-coated membranes.

Indexed as

Adaptor Protein Complex 2Adaptor Protein Complex alpha SubunitsAdaptor Proteins, Vesicular TransportAnimalsBrain-Derived Neurotrophic FactorCell MembraneCells, CulturedClathrinClathrin Heavy ChainsEndocytosisHippocampusHumansMembrane ProteinsMiceNerve Growth FactorNeuronsAdaptor Protein Complex 2Adaptor Protein Complex alpha SubunitsAdaptor Proteins, Vesicular TransportBrain-Derived Neurotrophic FactorClathrinClathrin Heavy ChainsMembrane ProteinsNerve Growth FactorReceptor, trkA

Identifiers

PMID11007890
PMCPMC6772792
OpenAlexW1577835340

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.