Evidence map›Paper›PMID 27126383›Full record

ReviewCurrent genetics2016

The long life of an endocytic patch that misses AP-2.

Nagore de León, M-Henar Valdivieso

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. The Ambivalent Function of YAP in Apoptosis and Cancer.International journal of molecular sciences · 2018
    Review
  7. Article
  8. 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

2 authors.

Nagore de LeónDepartamento de Microbiología y Genética/Instituto de Biología Funcional y Genómica (IBFG), University of Salamanca/CSIC, Calle Zacarías González 2, 37007, Salamanca, Spain.
M-Henar ValdiviesoDepartamento de Microbiología y Genética/Instituto de Biología Funcional y Genómica (IBFG), University of Salamanca/CSIC, Calle Zacarías González 2, 37007, Salamanca, Spain. henar@usal.es.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endocytosis is the process by which cells regulate extracellular fluid uptake and internalize molecules bound to their plasma membrane. This process requires the generation of protein-coated vesicles. In clathrin-mediated endocytosis (CME) the assembly polypeptide 2 (AP-2) adaptor facilitates rapid endocytosis of some plasma membrane receptors by mediating clathrin recruitment to the endocytic site and by connecting cargoes to the clathrin coat. While this adaptor is essential for early embryonic development in mammals, initial results suggested that it is dispensable for endocytosis in unicellular eukaryotes. The drastic effect of depleting AP-2 in metazoa and the mild effect of deleting AP-2 subunits in Saccharomyces cerevisiae have prevented a detailed analysis of the dynamics of endocytic patches in the absence of this adaptor. Using live-cell imaging of Schizosaccharomyces pombe endocytic sites we have shown that eliminating AP-2 perturbs the dynamics of endocytic patches beyond the moment of coat assembly. These perturbations affect the cell growth pattern and cell wall synthesis. Our results highlight the importance of using different model organisms to address the study of conserved aspects of CME.

Indexed as

ClathrinClathrin-Coated VesiclesEndocytosisSchizosaccharomycesTranscription Factor AP-2YeastsClathrinTranscription Factor AP-2AP-2Clathrin adaptorEndocytosisLive-cell imagingSchizosaccharomyces pombeYeast

Identifiers

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.