Evidence map›Paper›PMID 28792301›Full record

ArticleAutophagy2017

SQSTM1/p62-mediated autophagy compensates for loss of proteasome polyubiquitin recruiting capacity.

Alik Demishtein, Milana Fraiberg, Dikla Berko, Boaz Tirosh, Zvulun Elazar, Ami Navon

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
7.9field-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

61 citing papers in PubMed, 102 citations in OpenAlex.

  1. Article
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  4. Autophagy in ocular diseases: from mechanisms to therapeutic potential.Frontiers in cell and developmental biology · 2026
    Review
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  6. Review
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  12. Effects of invivo CXCR4 blockade and proteasome inhibition on bone marrow plasma cells in HLA-sensitized kidney transplant candidates.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2023
    Article
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  15. Review
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  18. Article
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  20. Article

1 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

6 authors at 2 institutions in 1 country.

Alik Demishteina Department of Biomolecular Sciences , The Weizmann Institute of Science , Rehovot , Israel.
Milana Fraiberga Department of Biomolecular Sciences , The Weizmann Institute of Science , Rehovot , Israel.
Dikla Berkob Department of Biological Regulation , The Weizmann Institute of Science , Rehovot , Israel.
Boaz Tiroshc Institute for Drug Research, The School of Pharmacy , Faculty of Medicine, The Hebrew University of Jerusalem , Jerusalem , Israel.
Zvulun Elazara Department of Biomolecular Sciences , The Weizmann Institute of Science , Rehovot , Israel.
Ami Navonb Department of Biological Regulation , The Weizmann Institute of Science , Rehovot , Israel.
Weizmann Institute of Science · ILHebrew University of Jerusalem · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein homeostasis in eukaryotic cells is regulated by 2 highly conserved degradative pathways, the ubiquitin-proteasome system (UPS) and macroautophagy/autophagy. Recent studies revealed a coordinated and complementary crosstalk between these systems that becomes critical under proteostatic stress. Under physiological conditions, however, the molecular crosstalk between these 2 pathways is still far from clear. Here we describe a cellular model of proteasomal substrate accumulation due to the combined knockdown of PSMD4/S5a and ADRM1, the 2 proteasomal ubiquitin receptors. This model reveals a compensatory autophagic pathway, mediated by a SQSTM1/p62-dependent clearance of accumulated polyubiquitinated proteins. In addition to mediating the sequestration of ubiquitinated cargos into phagophores, the precursors to autophagosomes, SQSTM1 is also important for polyubiquitinated aggregate formation upon proteasomal inhibition. Finally, we demonstrate that the concomitant stabilization of steady-state levels of ATF4, a rapidly degraded transcription factor, mediates SQSTM1 upregulation. These findings provide new insight into the molecular mechanisms by which selective autophagy is regulated in response to proteasomal overflow.

Indexed as

Adaptor Proteins, Signal TransducingAutophagyCells, CulturedHeLa CellsHumansPolyubiquitinProteasome Endopeptidase ComplexProtein BindingProteolysisSequestosome-1 ProteinUbiquitinated ProteinsUbiquitinationAdaptor Proteins, Signal TransducingPolyubiquitinProteasome Endopeptidase ComplexSequestosome-1 ProteinSQSTM1 protein, humanUbiquitinated ProteinsADRM1/Rpn13autophagyproteasomeSQSTM1/p62ubiquitin receptor PSMD4/Rpn10

Identifiers

PMID28792301
PMCPMC5640208
OpenAlexW2744359167

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.