Evidence map›Paper›PMID 30499183›Full record

ReviewThe FEBS journal2019

p62/SQSTM1: 'Jack of all trades' in health and cancer.

Pablo Sánchez-Martín, Tetsuya Saito, Masaaki Komatsu

Open access · hybridAbstract readReview
In one paragraph

Review in The FEBS journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers.

0numbers the graph read from it
0cells of the map it votes in
145citing papers in PubMed
15.2field-weighted citation impact, top 1% 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

145 citing papers in PubMed, 239 citations in OpenAlex.

  1. Review
  2. Haematologica · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. The Roles of SQSTM1/p62 in Selective Autophagy and Oncogenic Signaling.International journal of molecular sciences · 2026
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. DHRS9 promotes malignant progression of ovarian cancer through SQSTM1.Journal of cancer research and clinical oncology · 2025
    Article
  20. Review

85 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Pablo Sánchez-MartínDepartment of Biochemistry, Niigata University Graduate School of Medical and Dental Sciences, Japan.
Tetsuya SaitoDepartment of Biochemistry, Niigata University Graduate School of Medical and Dental Sciences, Japan.
Masaaki KomatsuDepartment of Biochemistry, Niigata University Graduate School of Medical and Dental Sciences, Japan.
Niigata University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

p62 is a stress-inducible protein able to change among binding partners, cellular localizations and form liquid droplet structures in a context-dependent manner. This protein is mainly defined as a cargo receptor for selective autophagy, a process that allows the degradation of detrimental and unnecessary components through the lysosome. Besides this role, its ability to interact with multiple binding partners allows p62 to act as a main regulator of the activation of the Nrf2, mTORC1, and NF-κB signaling pathways, linking p62 to the oxidative defense system, nutrient sensing, and inflammation, respectively. In the present review, we will present the molecular mechanisms behind the control p62 exerts over these pathways, their interconnection and how their deregulation contributes to cancer progression.

Indexed as

HumansInflammationNeoplasmsOxidative StressRNA-Binding ProteinsSequestosome-1 ProteinSignal TransductionP62 protein, humanRNA-Binding ProteinsSequestosome-1 ProteinSQSTM1 protein, humanautophagycancerKeap1mTORC1NF-κBNrf2p62/SQSTM1

Identifiers

PMID30499183
PMCPMC7379270
OpenAlexW2902644109

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.