Evidence map›Paper›PMID 42892647›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2026

TRIM36 catalyzes K63-linked ubiquitination of TAK1 to drive septic inflammation.

Shijie Song, Dingnai Nie, Zulaya Abudureyimu, Yijin Kuang, Wen Li, Xiaodan Yang, Qiao Ling, Junli Sheng, Huiru He, Xiaolong You and 6 more

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Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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5 · Who and what money

Authors and funding

16 authors.

Shijie Song *Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, The Second School of Clinical Medicine, The State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, China.
Dingnai Nie *Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, The Second School of Clinical Medicine, The State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, China.
Zulaya Abudureyimu *Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, The Second School of Clinical Medicine, The State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, China.
Yijin KuangSchool of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, China.
Wen LiGuangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, The Second School of Clinical Medicine, The State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, China.
Xiaodan YangGuangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, The Second School of Clinical Medicine, The State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, China.
Qiao LingGuangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, The Second School of Clinical Medicine, The State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, China.
Junli ShengGuangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, The Second School of Clinical Medicine, The State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, China.
Huiru HeGuangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, The Second School of Clinical Medicine, The State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, China.
Xiaolong YouGuangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, The Second School of Clinical Medicine, The State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, China.
Suwan WuGuangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, The Second School of Clinical Medicine, The State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, China.
Wenhao LuGuangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, The Second School of Clinical Medicine, The State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, China.
Yuling FuGuangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, The Second School of Clinical Medicine, The State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, China.
Shouhai WuDepartment of Nephrology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China. wushouhai@gzucm.edu.cn.
Kang ChenDepartment of Laboratory Medicine, Zhongshan City People's Hospital, Zhongshan, Guangdong, China. ck521620@163.com.
Shengfeng HuGuangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, The Second School of Clinical Medicine, The State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, China. hushengfeng@smu.edu.cn.ORCID https://orcid.org/0000-0001-7901-4410

Funding

Fund of the State Key Laboratory of Respiratory Diseases SKLRD-Z-202506Guangdong Special Support Plan for Young Top-notch Talent Project 2024TQ08A146National Natural Science Foundation of China 82471780National Natural Science Foundation of China 82603511the Research Fund of Health Commission of Guangdong Province A2023130the Research Fund of Health Commission of Guangdong Province B2023141the Science and Technology Fund of Guangdong Provincial Hospital of Chinese Medicine YN2024GZRPY048Zhongshan Scientific Research Special Project for the Inheritance and Innovative Development of Traditional Chinese Medicine 2024B3008Zhongshan's Third Batch of Social Welfare and Basic Research Projects 2023B3024
6 · The paper itself

Abstract

backgroundThe Toll-like receptor 4 (TLR4) pathway is critical for initiating innate immunity; however, its dysregulation drives pathological inflammation in diseases such as sepsis.

methodsIn the present study, we utilized septic patients, lipopolysaccharide (LPS)-induced mouse models, and LPS-treated mouse macrophages as well as human THP-1-derived macrophages to investigate the potential functions and molecular mechanisms of TRIM36 in sepsis.

resultsHere, we identify tripartite motif protein 36 (TRIM36) as a key positive regulator that amplifies TLR4 signaling. TRIM36 expression was robustly upregulated in macrophages upon lipopolysaccharide (LPS) challenge. Mechanistically, TRIM36 directly bound to TGF-β-activated kinase 1 (TAK1) and catalyzed its K63-linked ubiquitination, a prerequisite for the activation of TAK1 and the downstream nuclear factor-κB (NF-κB) pathway. Functionally, genetic ablation of Trim36 in mice attenuated hypothermia, improved survival, and reduced cytokine production in an LPS-induced sepsis model. Consistently, in vitro knockdown of TRIM36 in human macrophages blunted LPS-induced signaling and the secretion of proinflammatory mediators. Furthermore, analysis of a public transcriptomic dataset revealed that elevated TRIM36 levels were associated with non-survival in patients with sepsis.

conclusionsCollectively, our findings establish TRIM36 as a critical amplifier of TLR4-induced hyperinflammation and highlight its potential as a therapeutic target for sepsis.

Indexed as

MAP Kinase Kinase KinasesSepsisTripartite Motif ProteinsTristetraprolinAnimalsCytokinesFemaleHumansInflammationIntracellular Signaling Peptides and ProteinsLipopolysaccharidesMacrophagesMaleMAP Kinase Kinase Kinase 7MiceMice, Inbred C57BLCytokinesIntracellular Signaling Peptides and ProteinsLipopolysaccharidesMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesNF-kappa BTifab protein, humanToll-Like Receptor 4Tripartite Motif ProteinsTristetraprolinInflammasomeMacrophagesNF-κBSepsisUbiquitination

Identifiers

PMID42892647

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