Evidence map›Paper›PMID 33953350›Full record

ArticleCell death and differentiation2021

E3 ligase TRIM25 ubiquitinates RIP3 to inhibit TNF induced cell necrosis.

Pucheng Mei, Feiyan Xie, Jiasong Pan, Sen Wang, Wenqing Gao, Rui Ge, Baocai Gao, Siqi Gao, Xiangjun Chen, Yongming Wang and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Cell death and differentiation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.9field-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

42 citing papers in PubMed, 77 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

13 authors at 1 institution in 1 country.

Pucheng Mei *State Key Laboratory of Genetic Engineering, Department of Neurology, School of Life Sciences and Huashan Hospital, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, Fudan University, Shanghai, 200438, China.
Feiyan Xie *State Key Laboratory of Genetic Engineering, Department of Neurology, School of Life Sciences and Huashan Hospital, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, Fudan University, Shanghai, 200438, China.
Jiasong PanState Key Laboratory of Genetic Engineering, Department of Neurology, School of Life Sciences and Huashan Hospital, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, Fudan University, Shanghai, 200438, China.
Sen WangState Key Laboratory of Genetic Engineering, Department of Neurology, School of Life Sciences and Huashan Hospital, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, Fudan University, Shanghai, 200438, China.
Wenqing GaoState Key Laboratory of Genetic Engineering, Department of Neurology, School of Life Sciences and Huashan Hospital, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, Fudan University, Shanghai, 200438, China.
Rui GeState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, 200438, China.
Baocai GaoState Key Laboratory of Genetic Engineering, Department of Neurology, School of Life Sciences and Huashan Hospital, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, Fudan University, Shanghai, 200438, China.
Siqi GaoState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, 200438, China.
Xiangjun ChenDepartment of Neurology, Huashan Hospital, Fudan University, Shanghai, 200040, China.
Yongming WangState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, 200438, China.ORCID http://orcid.org/0000-0001-8269-5296
Jiaxue WuState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, 200438, China.ORCID http://orcid.org/0000-0003-2590-4914
Chen DingState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, 200438, China.
Jixi LiState Key Laboratory of Genetic Engineering, Department of Neurology, School of Life Sciences and Huashan Hospital, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, Fudan University, Shanghai, 200438, China. lijixi@fudan.edu.cn.ORCID http://orcid.org/0000-0003-3463-3175
Fudan University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82071782
6 · The paper itself

Abstract

Receptor interacting protein kinase 3 (RIP3 or RIPK3), the critical executor of cell programmed necrosis, plays essential roles in maintaining immune responses and appropriate tissue homeostasis. Although the E3 ligases CHIP and PELI1 are reported to promote RIP3 degradation, however, how post-translational modification regulates RIP3 activity and stability is poorly understood. Here, we identify the tripartite motif protein TRIM25 as a negative regulator of RIP3-dependent necrosis. TRIM25 directly interacts with RIP3 through its SPRY domain and mediates the K48-linked polyubiquitination of RIP3 on residue K501. The RING domain of TRIM25 facilitates the polyubiquitination chain on RIP3, thereby promoting proteasomal degradation of RIP3. Also, TRIM25 deficiency inhibited the ubiquitination of RIP3, thus promoting TNF-induced cell necrosis. Our current finding reveals the regulating mechanism of polyubiquitination on RIP3, which might be a potential therapeutic target for the intervention of RIP3-dependent necrosis-related diseases.

Indexed as

HumansNecrosisPeptide FragmentsReceptor-Interacting Protein Serine-Threonine KinasesSignal TransductionTranscription FactorsTransfectionTripartite Motif ProteinsTumor Necrosis Factor-alphaUbiquitinationUbiquitin-Protein LigasesPeptide FragmentsReceptor-Interacting Protein Serine-Threonine KinasesRIPK3 protein, humanTranscription FactorsTRIM25 protein, humanTripartite Motif Proteinstumor necrosis factor (1-26)Tumor Necrosis Factor-alphaUbiquitin-Protein Ligases

Identifiers

PMID33953350
PMCPMC8481267
OpenAlexW3157705058

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.