Evidence map›Paper›PMID 27325701›Full record

ArticleThe Journal of biological chemistry2016

Sequestosome 1/p62 Protein Is Associated with Autophagic Removal of Excess Hepatic Endoplasmic Reticulum in Mice.

Hua Yang, Hong-Min Ni, Fengli Guo, Yifeng Ding, Ying-Hong Shi, Pooja Lahiri, Leopold F Fröhlich, Thomas Rülicke, Claudia Smole, Volker C Schmidt and 5 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
7.6field-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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Autophagy in the liver.Autophagy reports · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. The mechanisms and roles of selective autophagy in mammals.Nature reviews. Molecular cell biology · 2023
    Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. 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

15 authors at 8 institutions in 5 countries.

Hua YangFrom the Department of Liver Surgery, Liver Cancer Institute, Zhongshan Hospital, Fudan University, Shanghai 20032, China, the Department of Pharmacology, Toxicology, and Therapeutics, University of Kansas Medical Center, Kansas City, Kansas 66160.
Hong-Min Nithe Department of Pharmacology, Toxicology, and Therapeutics, University of Kansas Medical Center, Kansas City, Kansas 66160.
Fengli Guothe Stowers Institute for Medical Research, Kansas City, Missouri 64110.
Yifeng Dingthe Department of Pharmacology, Toxicology, and Therapeutics, University of Kansas Medical Center, Kansas City, Kansas 66160.
Ying-Hong ShiFrom the Department of Liver Surgery, Liver Cancer Institute, Zhongshan Hospital, Fudan University, Shanghai 20032, China.
Pooja Lahirithe Institute of Pathology, Medical University of Graz, A-8036 Graz, Austria.
Leopold F Fröhlichthe Department of Cranio-Maxillofacial Surgery, University of Münster, Albert-Schweitzer-Campus 1, 48149 Münster, Germany.
Thomas Rülickethe Institute of Laboratory Animal Science and Biomodels Austria, University of Veterinary Medicine, 1210 Vienna, Austria.
Claudia Smolethe Institute of Pathology, Medical University of Graz, A-8036 Graz, Austria.
Volker C Schmidtthe Institute of Laboratory Animal Science and Biomodels Austria, University of Veterinary Medicine, 1210 Vienna, Austria.
Kurt Zatloukalthe Institute of Pathology, Medical University of Graz, A-8036 Graz, Austria.
Yue Cuithe Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, Washington 98159, and.
Masaaki Komatsuthe Department of Biochemistry, School of Medicine, Niigata University, Chuo-ku, Niigata 951-8510, Japan.
Jia FanFrom the Department of Liver Surgery, Liver Cancer Institute, Zhongshan Hospital, Fudan University, Shanghai 20032, China, fan.jia@zs-hospital.sh.cn.
Wen-Xing Dingthe Department of Pharmacology, Toxicology, and Therapeutics, University of Kansas Medical Center, Kansas City, Kansas 66160, wxding@kumc.edu.
Fudan University · CNMedical University of Graz · ATUniversity of Kansas Medical Center · USUniversity of Veterinary Medicine Vienna · ATNiigata University · JPStowers Institute for Medical Research · USUniversity Hospital Münster · DEUniversity of Washington · US

Funding

THE ROLE OF HUMAN PXR IN ANTI-TUBERCULOSIS DRUG-INDUCED LIVER INJURYP20RR021940 · NCRR · UNIVERSITY OF KANSAS MEDICAL CENTER · PI JAESCHKE, HARTMUT W. · 2006 to 2011
$12.1M
Transgenic and Gener-Targeting CoreP20GM104936 · NIGMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI TRAN, PAMELA VIVIAN · 2012 to 2016
$10.9M
Nuclear Receptors in Liver Health and DiseaseP20GM103549 · NIGMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI JAESCHKE, HARTMUT W. · 2012 to 2015
$8.1M
Autophagy and Drug-Induced Liver InjuryR01DK102142 · NIDDK · UNIVERSITY OF KANSAS MEDICAL CENTER · PI DING, WEN-XING, JAESCHKE, HARTMUT W. · 2014 to 2022
$2.7M
Mechanisms regulating autophagy in alcohol-induced liver injuryR01AA020518 · NIAAA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI DING, WEN-XING · 2011 to 2018
$2.3M
JEOL JEM-1400 Transmission Electron Microscope with AMT-XR611M Digital Camera SysS10RR027564 · NCRR · UNIVERSITY OF KANSAS MEDICAL CENTER · PI ABRAHAMSON, DALE R · 2010 to 2010
$418k
Austrian Science Fund FWF W 1226NCRR NIH HHS P20 RR021940NCRR NIH HHS S10 RR027564NIAAA NIH HHS R01 AA020518NIDDK NIH HHS R01 DK102142NIGMS NIH HHS P20 GM103549NIGMS NIH HHS P20 GM104936
6 · The paper itself

Abstract

Xenobiotics exposure increases endoplasmic reticulum (ER) proliferation and cytochrome P-450 (CYP) induction to sustain metabolic requirements. Whether autophagy is essential for the removal of excess ER and CYP and whether an autophagy receptor is involved in this process in mammals remains elusive. In this study, we show that autophagy is induced in mouse livers after withdrawal of the hepatic mitogen 1,4-bis[2-(3,5-dichloropyridyloxy)] benzene (TCPOBOP). Although isolated autophagosomes, autolysosomes, and lysosomes from mouse livers after withdrawal of TCPOBOP contained ER proteins, those in control mouse livers did not. Liver-specific Atg5 knockout mice had higher basal hepatic ER content that was further increased and sustained after withdrawal of TCPOBOP compared with wild-type mice. In addition to regulating ER degradation, our results also suggest that autophagy plays a role in regulating the homeostasis of hepatic CYP because blocking autophagy led to increased CYP2B10 accumulation either at the basal level or following TCPOBOP withdrawal. Furthermore, we found that the autophagy receptor protein sequestosome 1 (SQSTM1)/p62 is associated with the ER. After withdrawal of TCPOBOP, p62 knockout mice had increased ER content in the liver compared with wild-type mice. These results suggest that p62 may act as an autophagy receptor for the autophagic removal of excess ER in the mouse liver. Taken together, our results indicate that autophagy is important for the removal of excess ER and hepatic CYP enzymes in mouse livers, a process associated with the autophagy receptor protein p62.

Indexed as

AutophagyAnimalsAryl Hydrocarbon HydroxylasesAutophagy-Related Protein 5Cytochrome P450 Family 2Endoplasmic ReticulumLiverMiceMice, KnockoutPyridinesSequestosome-1 ProteinSteroid Hydroxylases1,4-bis(2-(3,5-dichloropyridyloxy))benzeneAryl Hydrocarbon HydroxylasesAtg5 protein, mouseAutophagy-Related Protein 5Cyp2b10 protein, mouseCytochrome P450 Family 2PyridinesSequestosome-1 ProteinSqstm1 protein, mouseSteroid Hydroxylasesautophagycytochrome P-450endoplasmic reticulum (ER)liverp62 (sequestosome 1 (SQSTM1))

Identifiers

PMID27325701
PMCPMC5009243
OpenAlexW2470601847

What OpenQuestion holds

Textmetadata
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.