Evidence map›Paper›PMID 26381214›Full record

ArticleNature communications2015

Regulation of NKT cell-mediated immune responses to tumours and liver inflammation by mitochondrial PGAM5-Drp1 signalling.

Young Jun Kang, Bo-Ram Bang, Kyung Ho Han, Lixin Hong, Eun-Jin Shim, Jianhui Ma, Richard A Lerner, Motoyuki Otsuka

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed, 1 pooled it
5.4field-weighted citation impact, top 4% 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

100 citing papers in PubMed, 1 synthesis or guideline pooled it, 143 citations in OpenAlex.

  1. Interaction of HIF-1a with various cell death pathways in tumor immune microenvironment (TIME).Apoptosis : an international journal on programmed cell death · 2026
    Pooled it
  2. Programmed cell death in lung cancer: mechanisms, immune responses, and therapeutics.Apoptosis : an international journal on programmed cell death · 2026
    Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. The dual role of PGAM5 in inflammation.Experimental & molecular medicine · 2025
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Induced Necroptosis and Its Role in Cancer Immunotherapy.International journal of molecular sciences · 2024
    Review
  18. Article
  19. Article
  20. Review

40 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 2 countries.

Young Jun KangDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, California 92037, USA.
Bo-Ram BangDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, California 92037, USA.
Kyung Ho HanDepartment of Cell and Molecular Biology, The Scripps Research Institute, La Jolla, California 92037, USA.
Lixin HongDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, California 92037, USA.
Eun-Jin ShimDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, California 92037, USA.
Jianhui MaDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, California 92037, USA.
Richard A LernerDepartment of Cell and Molecular Biology, The Scripps Research Institute, La Jolla, California 92037, USA.
Motoyuki OtsukaDepartment of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo 113-0033, Japan.ORCID http://orcid.org/0000-0003-2869-2881
Scripps Research Institute · USUniversity of Tokyo Hospital · JP

Funding

Mechanism of 4-1BBL-mediated sustained inflammation: target of anti-inflammationR01AI088229 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI KANG, YOUNG JUN · 2010 to 2014
$2.1M
NIAID NIH HHS AI088229NIAID NIH HHS HHSN272201300006CNIAID NIH HHS R01 AI088229PHS HHS HHSN272201300006C
6 · The paper itself

Abstract

The receptor-interacting protein kinase 3 (RIPK3) plays crucial roles in programmed necrosis and innate inflammatory responses. However, a little is known about the involvement of RIPK3 in NKT cell-mediated immune responses. Here, we demonstrate that RIPK3 plays an essential role in NKT cell function via activation of the mitochondrial phosphatase phosphoglycerate mutase 5 (PGAM5). RIPK3-mediated activation of PGAM5 promotes the expression of cytokines by facilitating nuclear translocation of NFAT and dephosphorylation of dynamin-related protein 1 (Drp1), a GTPase is essential for mitochondrial homoeostasis. Ripk3(-/-) mice show reduced NKT cell responses to metastatic tumour cells, and both deletion of RIPK3 and pharmacological inhibition of Drp1 protects mice from NKT cell-mediated induction of acute liver damage. Collectively, the results identify a crucial role for RIPK3-PGAM5-Drp1/NFAT signalling in NKT cell activation, and further suggest that RIPK3-PGAM5 signalling may mediate crosstalk between mitochondrial function and immune signalling.

Indexed as

Active Transport, Cell NucleusAnimalsBlotting, WesternCytokinesDynaminsHEK293 CellsHepatocytesHumansImmunity, CellularInflammationInterferon-gammaInterleukin-4Jurkat CellsLiverMelanoma, ExperimentalMiceCytokinesDnm1l protein, mouseDynaminsInterferon-gammaInterleukin-4NFATC Transcription FactorsPGAM5 protein, mousePhosphoprotein PhosphatasesPhosphoric Monoester HydrolasesReceptor-Interacting Protein Serine-Threonine KinasesRipk3 protein, mouseTumor Necrosis Factor-alpha

Identifiers

PMID26381214
PMCPMC4576739
OpenAlexW2187131378

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.