Evidence map›Paper›PMID 28910396›Full record

ArticlePloS one2017

PI3K-C2α knockdown decreases autophagy and maturation of endocytic vesicles.

Nathan M Merrill, Joshua L Schipper, Jonathan B Karnes, Audra L Kauffman, Katie R Martin, Jeffrey P MacKeigan

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

16 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. C/EBPJournal of immunology research · 2022
    Article
  9. An Overview of Class II Phosphoinositide 3-Kinases.Current topics in microbiology and immunology · 2022
    Article
  10. Article
  11. Review
  12. Polyphosphate is an extracellular signal that can facilitate bacterial survival in eukaryotic cells.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  13. Review
  14. Review
  15. Aging · 2019
    Article
  16. 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

6 authors at 1 institution in 1 country.

Nathan M MerrillVan Andel Institute Graduate School, Grand Rapids, Michigan, United States of America.
Joshua L SchipperCenter for Cancer Cell Biology, Van Andel Research Institute, Grand Rapids, Michigan, United States of America.
Jonathan B KarnesVan Andel Institute Graduate School, Grand Rapids, Michigan, United States of America.
Audra L KauffmanCenter for Cancer Cell Biology, Van Andel Research Institute, Grand Rapids, Michigan, United States of America.
Katie R MartinCenter for Cancer Cell Biology, Van Andel Research Institute, Grand Rapids, Michigan, United States of America.
Jeffrey P MacKeiganVan Andel Institute Graduate School, Grand Rapids, Michigan, United States of America.ORCID http://orcid.org/0000-0002-0198-5679
Van Andel Institute · US

Funding

Computational Model of Autophagy-Mediated Survival in Chemoresistant Lung CancerR01CA197398 · NCI · VAN ANDEL RESEARCH INSTITUTE · PI HLAVACEK, WILLIAM S, MACKEIGAN, JEFFREY PAUL · 2015 to 2019
$2.5M
NCI NIH HHS R01 CA197398
6 · The paper itself

Abstract

Phosphoinositide 3-kinase (PI3K) family members are involved in diverse cellular fates including cell growth, proliferation, and survival. While many molecular details are known about the Class I and III PI3Ks, less is known about the Class II PI3Ks. To explore the function of all eight PI3K isoforms in autophagy, we knock down each gene individually and measure autophagy. We find a significant decrease in autophagy following siRNA-mediated PIK3C2A (encoding the Class 2 PI3K, PI3K-C2α) knockdown. This defective autophagy is rescued by exogenous PI3K-C2α, but not kinase-dead PI3K-C2α. Using confocal microscopy, we probe for markers of endocytosis and autophagy, revealing that PI3K-C2α colocalizes with markers of endocytosis. Though endocytic uptake is intact, as demonstrated by transferrin labeling, PIK3C2A knockdown results in vesicle accumulation at the recycling endosome. We isolate distinct membrane sources and observe that PI3K-C2α interacts with markers of endocytosis and autophagy, notably ATG9. Knockdown of either PIK3C2A or ATG9A/B, but not PI3KC3, results in an accumulation of transferrin-positive clathrin coated vesicles and RAB11-positive vesicles at the recycling endosome. Taken together, these results support a role for PI3K-C2α in the proper maturation of endosomes, and suggest that PI3K-C2α may be a critical node connecting the endocytic and autophagic pathways.

Indexed as

AutophagyBiomarkersCell LineCell ProliferationEndocytosisEndosomesGene Knockdown TechniquesHumansPhosphatidylinositol 3-KinasesRNA, Small InterferingSignal TransductionTransport VesiclesBiomarkersPhosphatidylinositol 3-KinasesPIK3C2A protein, humanRNA, Small Interfering

Identifiers

PMID28910396
PMCPMC5599018
OpenAlexW2754367256

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.