Evidence map›Paper›PMID 28059602›Full record

ArticleCell cycle (Georgetown, Tex.)2017

SUMOylation of KLF4 promotes IL-4 induced macrophage M2 polarization.

Kezhou Wang, Wei Zhou, Qi Cai, Jinke Cheng, Rong Cai, Rong Xing

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

30 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Immune regulation by the SUMO family.Nature reviews. Immunology · 2025
    Review
  6. Article
  7. Review
  8. KLF feedback loops in innate immunity.Frontiers in immunology · 2025
    Review
  9. Retinoic acid ameliorates rheumatoid arthritis by attenuating inflammation and modulating macrophage polarization through MKP-1/MAPK signaling pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Article
  10. Review
  11. Article
  12. Article
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  14. Review
  15. Article
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  17. Article
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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

6 authors at 2 institutions in 1 country.

Kezhou Wanga Department of Biochemistry and Molecular Cell Biology , Shanghai Jiaotong University School of Medicine , Shanghai , China.
Wei Zhoua Department of Biochemistry and Molecular Cell Biology , Shanghai Jiaotong University School of Medicine , Shanghai , China.
Qi Caia Department of Biochemistry and Molecular Cell Biology , Shanghai Jiaotong University School of Medicine , Shanghai , China.
Jinke Chenga Department of Biochemistry and Molecular Cell Biology , Shanghai Jiaotong University School of Medicine , Shanghai , China.
Rong Caia Department of Biochemistry and Molecular Cell Biology , Shanghai Jiaotong University School of Medicine , Shanghai , China.
Rong Xingb Department of Pathophysiology , Dalian Medical University , Dalian , China.
Shanghai Jiao Tong University · CNDalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages, in response to different environmental cues, undergo the classical polarization (M1 macrophages) as well as the alternative polarization (M2 macrophages) that involve the functions of stimulus-specific transcription factors. Kruppel-like factor 4 (KLF4), a member of a subfamily of the zinc-finger class of DNA-binding transcription factors, plays as a critical regulator of macrophage polarization. KLF4 has been reported as a SUMOylated protein. In this study, we showed that SUMOylation of KLF4, is induced by IL-4 treatment in macrophages. IL4-induced KLF4 SUMOylation promotes RAW264.7 cells and bone marrow derived macrophages (BMDMs) to polarize into M2 subset. Thus, we identified an important post-translational modification (PTM), SUMOylation, plays a crucial role in regulating KLF4 activity during IL-4 induced macrophage M2 polarization. SUMOylation of KLF4 can be a potential therapeutic target in the resolution of inflammation.

Indexed as

AnimalsArginaseCell LineCell PolarityHumansInterleukin-4Kruppel-Like Factor 4Kruppel-Like Transcription FactorsMacrophagesMiceModels, BiologicalPromoter Regions, GeneticProtein BindingSumoylationArginaseInterleukin-4KLF4 protein, humanKlf4 protein, mouseKruppel-Like Factor 4Kruppel-Like Transcription Factorsalternative polarizationIL-4Kruppel-like factor 4 (KLF4)macrophageSUMOylation

Identifiers

PMID28059602
PMCPMC5324751
OpenAlexW2569222598

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.