Evidence map›Paper›PMID 35173167›Full record

ArticleNature communications2022

The AUTOTAC chemical biology platform for targeted protein degradation via the autophagy-lysosome system.

Chang Hoon Ji, Hee Yeon Kim, Min Ju Lee, Ah Jung Heo, Daniel Youngjae Park, Sungsu Lim, Seulgi Shin, Srinivasrao Ganipisetti, Woo Seung Yang, Chang An Jung and 12 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 153 papers.

0numbers the graph read from it
0cells of the map it votes in
153citing papers in PubMed
23.6field-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

153 citing papers in PubMed, 297 citations in OpenAlex.

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  17. The AUTACE That Degrades KRAS and Engages CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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93 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

22 authors at 5 institutions in 3 countries.

Chang Hoon Ji *Cellular Degradation Biology Center and Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, 03080, Korea.
Hee Yeon Kim *Cellular Degradation Biology Center and Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, 03080, Korea.ORCID http://orcid.org/0000-0002-3628-5576
Min Ju Lee *Cellular Degradation Biology Center and Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, 03080, Korea.
Ah Jung HeoCellular Degradation Biology Center and Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, 03080, Korea.
Daniel Youngjae ParkCellular Degradation Biology Center and Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, 03080, Korea.
Sungsu LimConvergence Research Center for Brain Science, Brain Science Institute, Korea Institute of Science and Technology (KIST), Seoul, 02792, Korea.
Seulgi ShinConvergence Research Center for Brain Science, Brain Science Institute, Korea Institute of Science and Technology (KIST), Seoul, 02792, Korea.
Srinivasrao GanipisettiBrown Cancer Center, University of Louisville, 529 S Jackson Street, Louisville, KY, 40202, USA.
Woo Seung YangConvergence Research Center for Brain Science, Brain Science Institute, Korea Institute of Science and Technology (KIST), Seoul, 02792, Korea.
Chang An JungAUTOTAC Bio Inc., Changkkyunggung-ro 254, Jongno-gu, Seoul, 03080, Korea.
Kun Young KimAUTOTAC Bio Inc., Changkkyunggung-ro 254, Jongno-gu, Seoul, 03080, Korea.
Eun Hye JeongAUTOTAC Bio Inc., Changkkyunggung-ro 254, Jongno-gu, Seoul, 03080, Korea.
Sun Ho ParkAUTOTAC Bio Inc., Changkkyunggung-ro 254, Jongno-gu, Seoul, 03080, Korea.
Su Bin KimCellular Degradation Biology Center and Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, 03080, Korea.
Su Jin LeeCellular Degradation Biology Center and Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, 03080, Korea.
Jeong Eun NaAUTOTAC Bio Inc., Changkkyunggung-ro 254, Jongno-gu, Seoul, 03080, Korea.
Ji In KangAnticancer Agents Research Center, Korea Research Institute of Bioscience and Biotechnology, Ochang, Cheongju, 28116, Korea.ORCID http://orcid.org/0000-0002-9250-2053
Hyung Min ChiDepartment of Chemisty, Pohang University of Science and Technology, Pohang, 37673, Korea.
Hyun Tae KimAUTOTAC Bio Inc., Changkkyunggung-ro 254, Jongno-gu, Seoul, 03080, Korea.
Yun Kyung KimConvergence Research Center for Brain Science, Brain Science Institute, Korea Institute of Science and Technology (KIST), Seoul, 02792, Korea. yunkyungkim@kist.re.kr.ORCID http://orcid.org/0000-0002-8682-120X
Bo Yeon KimAnticancer Agents Research Center, Korea Research Institute of Bioscience and Biotechnology, Ochang, Cheongju, 28116, Korea. bykim@kribb.re.kr.ORCID http://orcid.org/0000-0003-1105-5480
Yong Tae KwonCellular Degradation Biology Center and Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, 03080, Korea. yok5@snu.ac.kr.ORCID http://orcid.org/0000-0002-8115-3150
Seoul National University · KRKorea Institute of Brain Science · KRKorea Research Institute of Bioscience and Biotechnology · KRPohang University of Science and Technology · KRUniversity of Louisville · US

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 degraders that harness the proteasome or the lysosome have been developed, a technology that simultaneously degrades targets and accelerates cellular autophagic flux is still missing. In this study, we develop a general chemical tool and platform technology termed AUTOphagy-TArgeting Chimera (AUTOTAC), which employs bifunctional molecules composed of target-binding ligands linked to autophagy-targeting ligands. AUTOTACs bind the ZZ domain of the otherwise dormant autophagy receptor p62/Sequestosome-1/SQSTM1, which is activated into oligomeric bodies in complex with targets for their sequestration and degradation. We use AUTOTACs to degrade various oncoproteins and degradation-resistant aggregates in neurodegeneration at nanomolar DC

Indexed as

ProteolysisAutophagyCell Line, TumorHeLa CellsHumansLysosomesOncogene ProteinsProtein AggregatesProtein BindingProtein FoldingProteostasisSignal TransductionOncogene ProteinsProtein Aggregates

Identifiers

PMID35173167
PMCPMC8850458
OpenAlexW4213121119

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.