Evidence map›Paper›PMID 31339911›Full record

ArticlePloS one2019

A cell-based assay for CD63-containing extracellular vesicles.

Anil G Cashikar, Phyllis I Hanson

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

36 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
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  5. Article
  6. Endosome transcriptomics reveal trafficking of Cajal bodies into multivesicular bodies.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  7. Article
  8. Autophagic stress activates distinct compensatory secretory pathways in neurons.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Exploiting the biogenesis of extracellular vesicles for bioengineering and therapeutic cargo loading.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    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

2 authors at 1 institution in 1 country.

Anil G CashikarDepartment of Cell Biology & Physiology, Washington University School of Medicine, St. Louis, Missouri, United States of America.ORCID 0000-0002-3671-684X
Phyllis I HansonDepartment of Cell Biology & Physiology, Washington University School of Medicine, St. Louis, Missouri, United States of America.
Washington University in St. Louis · US

Funding

ANALYSIS OF ESCRT FUNCTION IN ENDOLYSOSOMAL TRAFFICKINGR01GM122434 · NIGMS · WASHINGTON UNIVERSITY · PI HANSON, PHYLLIS I · 2017 to 2024
$3.7M
MOLECULAR MECHANISMS OF MULTIVESICULAR BODY BIOGENESISR01GM076686 · NIGMS · WASHINGTON UNIVERSITY · PI HANSON, PHYLLIS I · 2008 to 2011
$1.6M
NIGMS NIH HHS R01 GM076686NIGMS NIH HHS R01 GM122434
6 · The paper itself

Abstract

Extracellular vesicles (EVs) are thought to be important in cell-cell communication and have elicited extraordinary interest as potential biomarkers of disease. However, quantitative methods to enable elucidation of mechanisms underlying release are few. Here, we describe a cell-based assay for monitoring EV release using the EV-enriched tetraspanin CD63 fused to the small, ATP-independent reporter enzyme, Nanoluciferase. Release of CD63-containing EVs from stably expressing cell lines was monitored by comparing luciferase activity in culture media to that remaining in cells. HEK293, U2OS, U87 and SKMel28 cells released 0.3%-0.6% of total cellular CD63 in the form of EVs over 5 hrs, varying by cell line. To identify cellular machinery important for secretion of CD63-containing EVs, we performed a screen of biologically active chemicals in HEK293 cells. While a majority of compounds did not significantly affect EV release, treating cells with the plecomacrolides bafilomycin or concanamycin, known to inhibit the V-ATPase, dramatically increased EV release. Interestingly, alkalization of the endosomal lumen using weak bases had no effect, suggesting a pH-independent enhancement of EV release by V-ATPase inhibitors. The ability to quantify EVs in small samples will enable future detailed studies of release kinetics as well as further chemical and genetic screening to define pathways involved in EV secretion.

Indexed as

Secretory PathwayCell Line, TumorEnzyme InhibitorsExocytosisExtracellular VesiclesGenes, ReporterHEK293 CellsHumansLuciferasesMacrolidesRecombinant ProteinsTetraspanin 30Vacuolar Proton-Translocating ATPasesEnzyme InhibitorsLuciferasesMacrolidesRecombinant ProteinsTetraspanin 30Vacuolar Proton-Translocating ATPases

Identifiers

PMID31339911
PMCPMC6655660
OpenAlexW2963146858

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.