Evidence map›Paper›PMID 28855251›Full record

ArticleThe Journal of cell biology2017

PICK1 regulates AMPA receptor endocytosis via direct interactions with AP2 α-appendage and dynamin.

Maria Fiuza, Christine M Rostosky, Gabrielle T Parkinson, Alexei M Bygrave, Nagaraj Halemani, Marcio Baptista, Ira Milosevic, Jonathan G Hanley

Open access · hybridAbstract read
In one paragraph

Article in The Journal of cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

41 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Amyloid-β-Driven Synaptic Deficits Are Mediated by Synaptic Removal of GluA3-Containing AMPA Receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Selective endocytosis of CaScience advances · 2022
    Article
  15. Article
  16. AMPA Receptor Function in Hypothalamic Synapses.Frontiers in synaptic neuroscience · 2022
    Review
  17. CaFrontiers in molecular neuroscience · 2022
    Article
  18. Article
  19. Synaptic tau: A pathological or physiological phenomenon?Acta neuropathologica communications · 2021
    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

8 authors at 2 institutions in 2 countries.

Maria FiuzaCentre for Synaptic Plasticity and School of Biochemistry, University of Bristol, Bristol, England, UK.
Christine M RostoskyEuropean Neuroscience Institute, University Medical Center Göttingen, Göttingen, Germany.ORCID 0000-0002-6903-5178
Gabrielle T ParkinsonCentre for Synaptic Plasticity and School of Biochemistry, University of Bristol, Bristol, England, UK.
Alexei M BygraveCentre for Synaptic Plasticity and School of Biochemistry, University of Bristol, Bristol, England, UK.
Nagaraj HalemaniCentre for Synaptic Plasticity and School of Biochemistry, University of Bristol, Bristol, England, UK.
Marcio BaptistaCentre for Synaptic Plasticity and School of Biochemistry, University of Bristol, Bristol, England, UK.
Ira MilosevicEuropean Neuroscience Institute, University Medical Center Göttingen, Göttingen, Germany.ORCID 0000-0001-6440-3763
Jonathan G HanleyCentre for Synaptic Plasticity and School of Biochemistry, University of Bristol, Bristol, England, UK jon.hanley@bristol.ac.uk.ORCID 0000-0003-1704-4707
University of Bristol · GBUniversitätsmedizin Göttingen · DE

Funding

Biotechnology and Biological Sciences Research CouncilMedical Research Council MR/L011131/1
6 · The paper itself

Abstract

Clathrin-mediated endocytosis (CME) is used to internalize a diverse range of cargo proteins from the cell surface, often in response to specific signals. In neurons, the rapid endocytosis of GluA2-containing AMPA receptors (AMPARs) in response to NMDA receptor (NMDAR) stimulation causes a reduction in synaptic strength and is the central mechanism for long-term depression, which underlies certain forms of learning. The mechanisms that link NMDAR activation to CME of AMPARs remain elusive. PICK1 is a BAR domain protein required for NMDAR-dependent reductions in surface GluA2; however, the molecular mechanisms involved are unclear. In this study, we show that PICK1 makes direct, NMDAR-dependent interactions with the core endocytic proteins AP2 and dynamin. PICK1-AP2 interactions are required for clustering AMPARs at endocytic zones in dendrites in response to NMDAR stimulation and for consequent AMPAR internalization. We further show that PICK1 stimulates dynamin polymerization. We propose that PICK1 is a cargo-specific endocytic accessory protein required for efficient, activity-dependent AMPAR endocytosis.

Indexed as

Adaptor Protein Complex 2AnimalsCarrier ProteinsCytoskeletal ProteinsDynaminsEndocytosisHEK293 CellsHumansNuclear ProteinsRatsRats, WistarReceptors, AMPAReceptors, N-Methyl-D-AspartateAdaptor Protein Complex 2Carrier ProteinsCytoskeletal ProteinsDynaminsglutamate receptor ionotropic, AMPA 2Nuclear ProteinsPICk1 protein, humanPICK1 protein, ratReceptors, AMPAReceptors, N-Methyl-D-Aspartate

Identifiers

PMID28855251
PMCPMC5626541
OpenAlexW2751422759

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.