TRIM37 negatively regulates inflammatory responses induced by virus infection via controlling TRAF6 ubiquitination.
Biochem Biophys Res Commun
; 556: 87-92, 2021 06 04.
Article
in English
| MEDLINE | ID: covidwho-1173393
ABSTRACT
Virus-induced cytokine storm has been a devastating actuality in clinic. The abnormal production of type I interferon (IFN-1) and upregulation of multiple cytokines induced strong inflammation and thus lead to shock and organ failure. As an E3 ubiquitin ligase, tripartite motif-containing 37 (TRIM37) regulates the ubiquitination of multiple proteins including TRAFs. RNA sequencing was performed to investigated the alteration of transcriptional profile of H1N1-infected patients. qRT-PCR assay was performed to investigate the RNA levels of certain genes. The group of immune cells was examined by the Flow cytometry analysis. H&E staining was applied to evaluate lung inflammation of WT and TRIM37-KO mice. ELISA assay was performed to demonstrate the alteration of multiple cytokines. The protein levels in NF-kB signaling was estimated by western blotting and immunoprecipitation assays were applied to demonstrate the direct interaction between TRIM37 and TRAF-6. The RNA level of TRIM37 decreased in CD11b+ cells of Flu-infected patients. Knockout of TRIM37 inhibited the immune responses of H1N1-infected mice. TRIM37 deficiency reduced the levels of virous proinflammatory cytokines in bone marrow derived macrophages (BMDMs). Mechanically, TRIM37 promoted the K63-linked ubiquitination of TRAF6. TRIM37 negatively regulated inflammatory responses induced by virus infection via promoting TRAF6 ubiquitination at K63.
Keywords
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Orthomyxoviridae Infections
/
Ubiquitin-Protein Ligases
/
TNF Receptor-Associated Factor 6
/
Ubiquitination
/
Tripartite Motif Proteins
/
Inflammation
Type of study:
Experimental Studies
Limits:
Animals
/
Female
/
Humans
Language:
English
Journal:
Biochem Biophys Res Commun
Year:
2021
Document Type:
Article
Affiliation country:
J.bbrc.2021.03.147
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