Evidence map›Paper›PMID 31225504›Full record

ArticleCell stress2019

The primary cilium protein folliculin is part of the autophagy signaling pathway to regulate epithelial cell size in response to fluid flow.

Naïma Zemirli, Asma Boukhalfa, Nicolas Dupont, Joëlle Botti, Patrice Codogno, Etienne Morel

Open access · goldAbstract read
In one paragraph

Article in Cell stress, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

11 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Autophagy and the primary cilium in cell metabolism: What's upstream?Frontiers in cell and developmental biology · 2022
    Review
  9. Primary cilia and the reciprocal activation of AKT and SMAD2/3 regulate stretch-induced autophagy in trabecular meshwork cells.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  10. Review
  11. 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 3 institutions in 1 country.

Naïma ZemirliInstitut Necker-Enfants Malades (INEM), INSERM U1151-CNRS UMR 8253.
Asma BoukhalfaInstitut Necker-Enfants Malades (INEM), INSERM U1151-CNRS UMR 8253.
Nicolas DupontInstitut Necker-Enfants Malades (INEM), INSERM U1151-CNRS UMR 8253.
Joëlle BottiInstitut Necker-Enfants Malades (INEM), INSERM U1151-CNRS UMR 8253.
Patrice CodognoInstitut Necker-Enfants Malades (INEM), INSERM U1151-CNRS UMR 8253.
Etienne MorelInstitut Necker-Enfants Malades (INEM), INSERM U1151-CNRS UMR 8253.
Institut Necker Enfants Malades · FRSorbonne Paris Cité · FRUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is a conserved molecular pathway directly involved in the degradation and recycling of intracellular components. Autophagy is associated with a response to stress situations, such as nutrients deficit, chemical toxicity, mechanical stress or microbial host defense. We have recently shown that primary cilium-dependent autophagy is important to control kidney epithelial cell size in response to fluid flow induced shear stress. Here we show that the ciliary protein folliculin (FLCN) actively participates to the signaling cascade leading to the stimulation of fluid flow-dependent autophagy upstream of the cell size regulation in HK2 kidney epithelial cells. The knockdown of FLCN induces a shortening of the primary cilium, inhibits the activation of AMPK and the recruitment of the autophagy protein ATG16L1 at the primary cilium. Altogether, our results suggest that FLCN is essential in the dialog between autophagy and the primary cilium in epithelial cells to integrate shear stress-dependent signaling.

Indexed as

autophagyfluid flowfolliculinprimary ciliumshear stress

Identifiers

PMID31225504
PMCPMC6551741
OpenAlexW2920242715

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.