Evidence map›Paper›PMID 35722947›Full record

ArticleAutophagy2022

Targeted protein degradation via the autophagy-lysosome system: AUTOTAC (AUTOphagy-TArgeting Chimera).

Chang Hoon Ji, Min Ju Lee, Hee Yeon Kim, Ah Jung Heo, Daniel Youngjae Park, Yun Kyung Kim, Bo Yeon Kim, Yong Tae Kwon

Open access · greenAbstract readComment
In one paragraph

Article in Autophagy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

21 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Tau degradation in Alzheimer's disease: Mechanisms and therapeutic opportunities.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. The androgen receptor-targeted proteolysis targeting chimera and other alternative therapeutic choices in overcoming the resistance to androgen deprivation treatment in prostate cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Chang Hoon JiCellular Degradation Biology Center, Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, Korea.ORCID 0000-0002-1315-838X
Min Ju LeeCellular Degradation Biology Center, Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, Korea.
Hee Yeon KimCellular Degradation Biology Center, Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, Korea.
Ah Jung HeoCellular Degradation Biology Center, Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, Korea.
Daniel Youngjae ParkCellular Degradation Biology Center, Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, Korea.
Yun Kyung KimConvergence Research Center for Brain Science, Brain Science Institute, Korea Institute of Science and Technology (KIST), Seoul, Korea.
Bo Yeon KimChemical Biology Research Center, Korea Research Institute of Bioscience and Biotechnology, Ochang, Cheongju, Korea.
Yong Tae KwonCellular Degradation Biology Center, Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, Korea.ORCID 0000-0002-8115-3150
Seoul National University · KRKorea Institute of Brain Science · KRKorea Research Institute of Bioscience and Biotechnology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Targeted protein degradation allows targeting undruggable proteins for therapeutic applications as well as eliminating proteins of interest for research purposes. While several types of degraders that harness the proteasome or the lysosome have been developed, a technology that simultaneously degrades targets and accelerates cellular autophagic flux remains unavailable. In this study, we developed a general chemical tool by which given intracellular proteins are targeted to macroautophagy for lysosomal degradation. This platform technology, termed AUTOTAC (AUTOphagy-TArgeting Chimera), employs bifunctional molecules composed of target-binding ligands (TBLs) linked to autophagy-targeting ligands (ATLs). Upon binding to targets via the TBL, the ATL binds the ZZ domain of the otherwise dormant autophagy receptor SQSTM1/p62 (sequestosome 1), which activates SQSTM1 associated with targets and sequesters them into oligomeric species for autophagic targeting and lysosomal degradation. AUTOTACs were used to degrade various oncoproteins or aggregation-prone proteins in neurodegeneration both

Indexed as

AutophagyProteolysisArginineLigandsLysosomesSequestosome-1 ProteinArginineLigandsSequestosome-1 ProteinChemical toolsN-degron pathwayneurodegenerationN-terminal arginylationproteinopathyprotein quality controlproteolysisselective autophagySQSTM1/p62targeted protein degradation (TPD)

Identifiers

PMID35722947
PMCPMC9397417
OpenAlexW4283124143

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.