Evidence map›Paper›PMID 27404485›Full record

ReviewFEBS letters2016

p62/SQSTM1-Dr. Jekyll and Mr. Hyde that prevents oxidative stress but promotes liver cancer.

Koji Taniguchi, Shinichiro Yamachika, Feng He, Michael Karin

Abstract readReview
In one paragraph

Review in FEBS letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
8.6field-weighted citation impact, top 2% 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

65 citing papers in PubMed, 123 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Melatonin AttenuatesInternational journal of molecular sciences · 2024
    Article
  6. Review
  7. Article
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  19. Article
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5 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

4 authors at 2 institutions in 2 countries.

Koji TaniguchiLaboratory of Gene Regulation and Signal Transduction, Departments of Pharmacology and Pathology, University of California San Diego, La Jolla, CA, USA.
Shinichiro YamachikaLaboratory of Gene Regulation and Signal Transduction, Departments of Pharmacology and Pathology, University of California San Diego, La Jolla, CA, USA.
Feng HeLaboratory of Gene Regulation and Signal Transduction, Departments of Pharmacology and Pathology, University of California San Diego, La Jolla, CA, USA.
Michael KarinLaboratory of Gene Regulation and Signal Transduction, Departments of Pharmacology and Pathology, University of California San Diego, La Jolla, CA, USA.
University of California, San Diego · USKeio University · JP

Funding

Yeast Genetics and Stress Response Genes-BiomedicalP42ES010337 · NIEHS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI TUKEY, ROBERT H · 2000 to 2022
$69.8M
Role of Inflammation in tumor promotion and progressionR01CA118165 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KARIN, MICHAEL · 2007 to 2016
$4.6M
ER stress and UPR in non-alcoholic steatohepatitis and hepatocellular carcinomaR01CA198103 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI KAUFMAN, RANDAL J. · 2016 to 2020
$3.4M
IKKalpha, autophagy, obesity and injury enhanced pancreatic cancerR01CA163798 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KARIN, MICHAEL · 2012 to 2016
$1.9M
NCI NIH HHS R01 CA118165NCI NIH HHS R01 CA163798NCI NIH HHS R01 CA198103NIEHS NIH HHS P42 ES010337
6 · The paper itself

Abstract

p62/SQSTM1 is a multifunctional signaling hub and autophagy adaptor with many binding partners, which allow it to activate mTORC1-dependent nutrient sensing, NF-κB-mediated inflammatory responses, and the NRF2-activated antioxidant defense. p62 recognizes polyubiquitin chains via its C-terminal domain and binds to LC3 via its LIR motif, thereby promoting the autophagic degradation of ubiquitinated cargos. p62 accumulates in many human liver diseases, including nonalcoholic steatohepatitis (NASH) and hepatocellular carcinoma (HCC), where it is a component of Mallory-Denk bodies and intracellular hyaline bodies. Chronic p62 elevation contributes to HCC development by preventing oncogene-induced senescence and death of cancer-initiating cells and enhancing their proliferation. In this review, we discuss p62-mediated signaling pathways and their roles in liver pathophysiology, especially NASH and HCC.

Indexed as

Carcinoma, HepatocellularFoodGene Expression Regulation, NeoplasticHumansInflammationLiver NeoplasmsMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesNF-kappa BNon-alcoholic Fatty Liver DiseaseOxidative StressSequestosome-1 ProteinTOR Serine-Threonine KinasesMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesNF-kappa BSequestosome-1 ProteinSQSTM1 protein, humanTOR Serine-Threonine KinasesautophagyHCCmTORC1NASHNF-κBNRF2p62/SQSTM1

Identifiers

PMID27404485
PMCPMC4983218
OpenAlexW2461534763

What OpenQuestion holds

Textmetadata
LicenceTDM
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.