Evidence map›Paper›PMID 33173725›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2020

KEAP1 Mutations Drive Tumorigenesis by Suppressing SOX9 Ubiquitination and Degradation.

Na Shao, Hong Huang, Muhammad Idris, Xu Peng, Feng Xu, Shiwu Dong, Chungang Liu

Open access · goldAbstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

18 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. The roles of KLHL family members in human cancers.American journal of cancer research · 2022
    Review
  16. Article
  17. Article
  18. KEAP1 Mutations Drive Tumorigenesis by Suppressing SOX9 Ubiquitination and Degradation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020
    Article
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

7 authors at 2 institutions in 2 countries.

Na ShaoDepartment of Biomedical Materials Science School of Biomedical Engineering Army Medical University Chongqing 400038 P.R. China.
Hong HuangCenter of Biological Therapy Southwest Hospital Army Medical University Chongqing 400038 P.R. China.
Muhammad IdrisInstitute of Molecular and Cell Biology Agency for Science Technology and Research (A:STAR) Singapore Singapore.
Xu PengInstitute of Molecular and Cell Biology Agency for Science Technology and Research (A:STAR) Singapore Singapore.
Feng XuInstitute of Molecular and Cell Biology Agency for Science Technology and Research (A:STAR) Singapore Singapore.
Shiwu DongDepartment of Biomedical Materials Science School of Biomedical Engineering Army Medical University Chongqing 400038 P.R. China.
Chungang LiuCenter of Biological Therapy Southwest Hospital Army Medical University Chongqing 400038 P.R. China.ORCID https://orcid.org/0000-0001-7413-5934
Agency for Science, Technology and Research · SGArmy Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcription factor SOX9 is frequently amplified in diverse advanced-stage human tumors. Its stability has been shown to be tightly controlled by ubiquitination-dependent proteasome degradation. However, the exact underlying molecular mechanisms remain unclear. This work reports that SOX9 protein abundance is regulated by the Cullin 3-based ubiquitin ligase KEAP1 via proteasome-mediated degradation. Loss-of-function mutations in KEAP1 compromise polyubiquitination-mediated SOX9 degradation, leading to increased protein levels, which facilitate tumorigenesis. Moreover, the loss of critical ubiquitination residues in SOX9, by either a SOX9 (ΔK2) truncation or K249R mutation, leads to elevated protein stability. Furthermore, it is shown that the KEAP1/SOX9 interaction is modulated by CKI

Indexed as

CKIγCullin 3DNA damageKEPA1mutationsSOX9

Identifiers

PMID33173725
PMCPMC7610265
OpenAlexW3091687991

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.