Evidence map›Paper›PMID 34244427›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2021

HIPK2 phosphorylates HDAC3 for NF-κB acetylation to ameliorate colitis-associated colorectal carcinoma and sepsis.

Fang Zhang, Linlin Qi, Qiuyun Feng, Baokai Zhang, Xiangyue Li, Chang Liu, Weiyun Li, Qiaojie Liu, Dan Yang, Yue Yin and 8 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. 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 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 6% 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, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. The gut as a central hub for multi-organ crosstalk in aging.Cellular and molecular life sciences : CMLS · 2026
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Histone deacetylases and their inhibitors in kidney diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. FBXO22 inhibits colitis and colorectal carcinogenesis by regulating the degradation of the S2448-phosphorylated form of mTOR.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 4 institutions in 2 countries.

Fang ZhangInstitute of Geriatrics, Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong), School of Medicine, Shanghai University, Shanghai 200444, China.ORCID 0000-0001-5622-0422
Linlin QiState Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China.ORCID 0000-0003-3151-5843
Qiuyun FengSchool of Life Sciences, Shanghai University, Shanghai 200444, China.
Baokai ZhangSchool of Life Sciences, Shanghai University, Shanghai 200444, China.
Xiangyue LiSchool of Life Sciences, Shanghai University, Shanghai 200444, China.
Chang LiuState Key Laboratory of Cell Biology, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, University of the Chinese Academy of Sciences, Shanghai 200031, China.
Weiyun LiState Key Laboratory of Cell Biology, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, University of the Chinese Academy of Sciences, Shanghai 200031, China.
Qiaojie LiuState Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China.
Dan YangState Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China.ORCID 0000-0002-7870-6383
Yue YinNational Facility for Protein Science in Shanghai, Zhangjiang Lab, Shanghai 201210, China.
Chao PengNational Facility for Protein Science in Shanghai, Zhangjiang Lab, Shanghai 201210, China.
Han WuDivision of Trauma Surgery, Department of Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.ORCID 0000-0002-7504-0926
Zhao-Hui TangDivision of Trauma Surgery, Department of Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.ORCID 0000-0002-3465-880X
Xi ZhouState Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China.ORCID 0000-0002-3846-5079
Zou XiangDepartment of Health Technology and Informatics, Hong Kong Polytechnic University, Hung Hom, Hong Kong.ORCID 0000-0003-3925-0296
Zhijiang ZhangSchool of Communication & Information Engineering, Shanghai University, Shanghai 200444, China.
Hongyan WangState Key Laboratory of Cell Biology, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, University of the Chinese Academy of Sciences, Shanghai 200031, China; weibinwhy@shu.edu.cn hongyanwang@sibcb.ac.cn.
Bin WeiInstitute of Geriatrics, Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong), School of Medicine, Shanghai University, Shanghai 200444, China; weibinwhy@shu.edu.cn hongyanwang@sibcb.ac.cn.ORCID 0000-0002-2731-489X
Chinese Academy of Sciences · CNShanghai University · CNTongji Hospital · CNHong Kong Polytechnic University · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although inflammation is critical for the clearance of pathogens, uncontrolled inflammation also contributes to the development of multiple diseases such as cancer and sepsis. Since NF-κB-mediated transactivation in the nucleus is pivotal downstream of various stimuli to induce inflammation, searching the nuclear-localized targets specifically regulating NF-κB activation will provide important therapeutic application. Here, we have identified that homeodomain-interacting protein kinase 2 (HIPK2), a nuclear serine/threonine kinase, increases its expression in inflammatory macrophages. Importantly, HIPK2 deficiency or overexpression could enhance or inhibit inflammatory responses in LPS-stimulated macrophages, respectively. HIPK2-deficient mice were more susceptible to LPS-induced endotoxemia and CLP-induced sepsis. Adoptive transfer of

Indexed as

AcetylationAnimalsCecumColitisColorectal NeoplasmsCytokinesEndotoxemiaHistone Deacetylase 3Histone Deacetylase InhibitorsHistone DeacetylasesHumansInflammationInflammation MediatorsLigationLipopolysaccharidesLysineCytokinesHipk2 protein, mouseHistone Deacetylase 3Histone Deacetylase InhibitorsHistone DeacetylasesInflammation MediatorsLipopolysaccharidesLysineNF-kappa BPhosphoserineProtein Serine-Threonine KinasesToll-Like Receptor 4Toll-Like Receptor 9Transcription Factor RelAcolon cancercytokine stormHDAC3 phosphorylationHIPK2p65 acetylation

Identifiers

PMID34244427
PMCPMC8285910
OpenAlexW3179910031

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.