Evidence map›Paper›PMID 35618833›Full record

ArticleNature immunology2022

KSHV-encoded ORF45 activates human NLRP1 inflammasome.

Xing Yang, Jingfan Zhou, Chengrong Liu, Yafei Qu, Weili Wang, Maggie Z X Xiao, Fanxiu Zhu, Zhenshan Liu, Qiming Liang

Abstract read
PubMed Publisher
In one paragraph

Article in Nature immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.0field-weighted citation impact, top 7% 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

34 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
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  12. Viral oncogenesis in cancer: from mechanisms to therapeutics.Signal transduction and targeted therapy · 2025
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. NLRP inflammasomes in health and disease.Molecular biomedicine · 2024
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 4 countries.

Xing Yang *Center for Immune-Related Diseases at Shanghai Institute of Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jingfan Zhou *Center for Immune-Related Diseases at Shanghai Institute of Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Chengrong Liu *Center for Immune-Related Diseases at Shanghai Institute of Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yafei QuCenter for Immune-Related Diseases at Shanghai Institute of Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Weili WangCenter for Immune-Related Diseases at Shanghai Institute of Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Maggie Z X XiaoFaculty of Medicine, University of Alberta, Edmonton, Alberta, Canada.ORCID http://orcid.org/0000-0002-7534-6079
Fanxiu ZhuDepartment of Biological Science, Florida State University, Tallahassee, FL, USA.ORCID http://orcid.org/0000-0002-4189-7008
Zhenshan LiuCenter for Immune-Related Diseases at Shanghai Institute of Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Qiming LiangCenter for Immune-Related Diseases at Shanghai Institute of Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. liangqiming@shsmu.edu.cn.ORCID http://orcid.org/0000-0003-4792-1547
Shanghai Jiao Tong University · CNFlorida State University · USUniversity of Alberta · CA

Funding

Role of KSHV ORF45 in Viral Immune Evasion &ReplicationR01DE016680 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI ZHU, FANXIU · 2005 to 2015
$2.5M
NIDCR NIH HHS R01 DE016680
6 · The paper itself

Abstract

At steady state, the NOD-like receptor (NLR)-containing pyrin domain (PYD) (NLRP)1 inflammasome is maintained in an auto-inhibitory complex by dipeptidyl peptidases 8 and 9 (DPP8 and DPP9) and is activated by pathogen-encoded proteases after infection. Here, we showed that the open reading frame (ORF)45 protein of the Kaposi's sarcoma-associated herpesvirus activated the human NLRP1 (hNLRP1) inflammasome in a non-protease-dependent manner, and we additionally showed that the Linker1 region of hNLRP1, situated between the PYD and NACHT domains, was required for the auto-inhibition and non-protease-dependent activation of hNLRP1. At steady state, the interaction between Linker1 and the UPA subdomain silenced the activation of hNLRP1 in auto-inhibitory complexes either containing DPP9 or not in a manner independent of DPP9. ORF45 binding to Linker1 displaced UPA from the Linker1-UPA complex and induced the release of the C-terminal domain of hNLRP1 for inflammasome assembly. The ORF45-dependent activation of the NLRP1 inflammasome was conserved in primates but was not observed for murine NLRP1b inflammasomes.

Indexed as

Herpesvirus 8, HumanInflammasomesAnimalsCARD Signaling Adaptor ProteinsHumansMiceNLR ProteinsViral ProteinsCARD Signaling Adaptor ProteinsInflammasomesNLRP1 protein, humanNLR ProteinsViral Proteins

Identifiers

PMID35618833
OpenAlexW4281632263

What Socratic 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 Socratic graph.