Cited by 135Liver physiology and pathologyAutophagy in Disease and TherapyLiver Disease Diagnosis and Treatment

Role of p62/SQSTM1 in liver physiology and pathogenesis

Open access
Manley, Sharon, Williams, Jessica A, Ding, Wen-Xing·2013·Experimental Biology and Medicine

Abstract

p62/sequestosome-1/A170/ZIP (hereafter referred to as p62) is a scaffold protein that has multiple functions, such as signal transduction, cell proliferation, cell survival, cell death, inflammation, tumourigenesis and oxidative stress response. While p62 is an autophagy substrate and is degraded by autophagy, p62 serves as an autophagy receptor for selective autophagic clearance of protein aggregates and organelles. Moreover, p62 functions as a signalling hub for various signalling pathways, including NF-κB, Nrf2 and mTOR. In this review, we discuss the pathophysiological role of p62 in the liver, including formation of hepatic inclusion bodies, cholestasis, obesity, insulin resistance, liver cell death and tumourigenesis.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1177/1535370213489446

Cites

150 of 150 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Research works printed but not linked: 1

  1. [98]Muller TD Lee SJ Jastroch M Kabra D Stemmer K Aichler M Abplanalp B Ananthakrishnan G Bhardwaj N Collins S Divanovic S Endele M Finan B Gao Y Habegger KM Hembree J Heppner KM Hofmann S Holland J Kuchler D Kutschke M Krishna R Lehti M Oelkrug R Ottaway N Perez-Tilve D Raver C Walch AK Schriever SC Speakman J Tseng YH Diaz-Meco M Pfluger PT Moscat J Tschop MH p62 Links beta-adrenergic input to mitochondrial function and thermogenesis The Journal of clinical investigation 2012 PMC3533288 23257354

Cited by

Sorted by citations

Authors
Manley, S., Williams, J. A., & Ding, W.-X.
Affiliations
University of Kansas Medical Center (US)
Corresponding author
Ding, Wen-Xing
Venue
Experimental Biology and Medicine
Published
2013-05
Volume
238
Issue
5
Pages
525-538
ISSN
  • 0071-3384 (ISSN-L)
  • 1535-3702
  • 1535-3699
OpenAlex
W1983413606
Cited by
135
References
150
Citations by year
2026: 1 · 2025: 9 · 2024: 11 · 2023: 11 · 2022: 9 · 2021: 9 · 2020: 13 · 2019: 9 · 2018: 14 · 2017: 13 · 2016: 13 · 2015: 11 · 2014: 10 · 2013: 2
FWCI
7.45
Type
journal article
Language
en
Open access
Locations
  • Experimental Biology and Medicine (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institute on Alcohol Abuse and Alcoholism (R01AA020518, R37AA020518)
  • National Institute of Environmental Health Sciences (T32ES007079)
  • National Center for Research Resources (P20RR021940)
Topics
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
  • Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
Keywords
p62, liver physiology, liver disease pathogenesis, selective autophagy, autophagy receptors, protein aggregates, cholestasis, obesity, insulin resistance, hepatocyte death, NF-κB signaling, Nrf2 signaling, mTOR signaling, oxidative stress
MeSH terms
Sequestosome-1 Protein, Animals, Autophagy, Cell Transformation, Neoplastic, Inclusion Bodies, Humans, Inflammation, Insulin Resistance, Liver, Liver Neoplasms, Neoplasm Proteins, Signal Transduction, NF-kappa B, Oxidative Stress, Adaptor Proteins, Signal Transducing, Cell Proliferation, NF-E2-Related Factor 2, TOR Serine-Threonine Kinases

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review