Evidence map›Paper›PMID 33114389›Full record

ReviewCells2020

Selective Autophagy by Close Encounters of the Ubiquitin Kind.

Anna Vainshtein, Paolo Grumati

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 43 citations in OpenAlex.

  1. Emerging mechanisms of ATG8-independent non-canonical autophagy.Journal of physiology and biochemistry · 2026
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  10. Regulation of autophagy-mediated pathways by diet, physical activity, and sleep in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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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 1 country.

Anna VainshteinCraft Science Inc., Toronto, ON L4J 7S2, Canada.ORCID 0000-0003-0368-5044
Paolo GrumatiTelethon Institute of Genetics and Medicine, 80078 Pozzuoli (NA), Italy.
Telethon Institute Of Genetics And Medicine · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy, a bulk degradation process within eukaryotic cells, is responsible for cellular turnover and nutrient liberation during starvation. Increasing evidence indicate that this process can be extremely discerning. Selective autophagy segregates and eliminates protein aggregates, damaged organelles, and invading organisms. The specificity of this process is largely mediated by post-translational modifications (PTMs), which are recognized by autophagy receptors. These receptors grant autophagy surgical precision in cargo selection, where only tagged substrates are engulfed within autophagosomes and delivered to the lysosome for proteolytic breakdown. A growing number of selective autophagy receptors have emerged including p62, NBR1, OPTN, NDP52, TAX1BP1, TOLLIP, and more continue to be uncovered. The most well-documented PTM is ubiquitination and selective autophagy receptors are equipped with a ubiquitin binding domain and an LC3 interacting region which allows them to physically bridge cargo to autophagosomes. Here, we review the role of ubiquitin and ubiquitin-like post-translational modifications in various types of selective autophagy.

Indexed as

AutophagyAnimalsApoptosis Regulatory ProteinsAutophagosomesEndoplasmic ReticulumHumansMitochondriaMitophagyProtein BindingProtein Processing, Post-TranslationalUbiquitinUbiquitinationApoptosis Regulatory ProteinsUbiquitinaggrephagycargo receptorsER-phagylipophagylysophagymitophagynucleophagyselective autophagyubiquitinxenophagy

Identifiers

PMID33114389
PMCPMC7693032
OpenAlexW3093975929

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.