Evidence map›Paper›PMID 28542134›Full record

ArticleCell death & disease2017

Phosphorylated CAV1 activates autophagy through an interaction with BECN1 under oxidative stress.

Jihoon Nah, Seung-Min Yoo, Sunmin Jung, Eun Il Jeong, Moonju Park, Bong-Kiun Kaang, Yong-Keun Jung

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.1field-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

47 citing papers in PubMed, 66 citations in OpenAlex.

  1. Trial
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  5. Cav-1 deficiency induces cardiac dysfunction via the AdipoR1-AMPK-mTOR autophagy pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  6. Review
  7. Review
  8. Characterization of Corneal Defects in ATG7-Deficient Mice.International journal of molecular sciences · 2025
    Article
  9. Article
  10. Caveolae: Metabolic Platforms at the Crossroads of Health and Disease.International journal of molecular sciences · 2025
    Review
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  12. Article
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  14. Article
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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

7 authors at 1 institution in 1 country.

Jihoon NahDepartment of Biological Sciences, Seoul National University, 1 Gwanak-ro, Seoul, Gwanak-gu 151-747, Korea.
Seung-Min YooDepartment of Biological Sciences, Seoul National University, 1 Gwanak-ro, Seoul, Gwanak-gu 151-747, Korea.
Sunmin JungDepartment of Biological Sciences, Seoul National University, 1 Gwanak-ro, Seoul, Gwanak-gu 151-747, Korea.
Eun Il JeongDepartment of Biological Sciences, Seoul National University, 1 Gwanak-ro, Seoul, Gwanak-gu 151-747, Korea.
Moonju ParkDepartment of Biological Sciences, Seoul National University, 1 Gwanak-ro, Seoul, Gwanak-gu 151-747, Korea.
Bong-Kiun KaangDepartment of Biological Sciences, Seoul National University, 1 Gwanak-ro, Seoul, Gwanak-gu 151-747, Korea.
Yong-Keun JungDepartment of Biological Sciences, Seoul National University, 1 Gwanak-ro, Seoul, Gwanak-gu 151-747, Korea.
Seoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CAV1/Caveolin1, an integral membrane protein, is involved in caveolae function and cellular signaling pathways. Here, we report that CAV1 is a positive regulator of autophagy under oxidative stress and cerebral ischemic injury. Treatment with hydrogen peroxide enhanced autophagy flux and caused the localization of BECN1 to the mitochondria, whereas these changes were impaired in the absence of CAV1. Among many autophagy signals, only LC3 foci formation in response to hydrogen peroxide was abolished by CAV1 deficiency. Under oxidative stress, CAV1 interacted with a complex of BECN1/VPS34 through its scaffolding domain, and this interaction facilitated autophagosome formation. Interestingly, the phosphorylation of CAV1 at tyrosine-14 was essential for the interaction with BECN1 and their localization to the mitochondria, and the activation of autophagy in response to hydrogen peroxide. In addition, the expression of a phosphatase PTPN1 reduced the phosphorylation of CAV1 and inhibited autophagy. Further, compared to that in wild-type mice, autophagy was impaired and cerebral infarct damage was aggravated in the brain of Cav1 knockout mice. These results suggest that the phosphorylated CAV1 functions to activate autophagy through binding to the BECN1/VPS34 complex under oxidative stress and to protect against ischemic damage.

Indexed as

AutophagyOxidative StressAnimalsBeclin-1BrainBrain IschemiaCaveolin 1Gene Knockdown TechniquesHEK293 CellsHeLa CellsHumansHydrogen PeroxideMice, KnockoutMitochondriaModels, BiologicalPhosphorylationBeclin-1Caveolin 1Hydrogen Peroxide

Identifiers

PMID28542134
PMCPMC5520747
OpenAlexW2619482403

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.