Evidence map›Paper›PMID 21189453›Full record

ReviewAutophagy2011

Selective autophagy mediated by autophagic adapter proteins.

Terje Johansen, Trond Lamark

Open access · bronzeAbstract readReview
In one paragraph

Review in Autophagy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 974 papers.

0numbers the graph read from it
0cells of the map it votes in
974citing papers in PubMed
88.8field-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

974 citing papers in PubMed, 1,700 citations in OpenAlex.

  1. Article
  2. Review
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  12. Regulation of Innate Immune Signaling by Autophagy.International journal of molecular sciences · 2026
    Review
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  19. Review
  20. Review

914 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

2 authors at 1 institution in 3 countries.

Terje JohansenMolecular Cancer Research Group, Institute of Medical Biology, University of Tromsø, Tromsø, Norway. terje.johansen@uit.no
Trond Lamark
UiT The Arctic University of Norway · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mounting evidence suggests that autophagy is a more selective process than originally anticipated. The discovery and characterization of autophagic adapters, like p62 and NBR1, has provided mechanistic insight into this process. p62 and NBR1 are both selectively degraded by autophagy and able to act as cargo receptors for degradation of ubiquitinated substrates. A direct interaction between these autophagic adapters and the autophagosomal marker protein LC3, mediated by a so-called LIR (LC3-interacting region) motif, their inherent ability to polymerize or aggregate as well as their ability to specifically recognize substrates are required for efficient selective autophagy. These three required features of autophagic cargo receptors are evolutionarily conserved and also employed in the yeast cytoplasm-to-vacuole targeting (Cvt) pathway and in the degradation of P granules in C. elegans. Here, we review the mechanistic basis of selective autophagy in mammalian cells discussing the degradation of misfolded proteins, p62 bodies, aggresomes, mitochondria and invading bacteria. The emerging picture of selective autophagy affecting the regulation of cell signaling with consequences for oxidative stress responses, tumorigenesis and innate immunity is also addressed.

Indexed as

AutophagyAdaptor Proteins, Signal TransducingAmino Acid SequenceAnimalsHumansMitochondriaModels, BiologicalMolecular Sequence DataSubstrate SpecificityUbiquitinationAdaptor Proteins, Signal Transducing

Identifiers

PMID21189453
PMCPMC3060413
OpenAlexW1992532731

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.