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TRIM21 knockout mouse livers show enhanced antioxidant capacity and decreased compensatory proliferation

ABSTRACT: Acute response to diethylnitrosamine treatment in TRIM21 wild-type and knockout mice were compared and differentially expressed genes were inendified at 48 hours

ORGANISM(S): Mus musculus

PROVIDER: GSE164369 | GEO | 2021/04/14

REPOSITORIES: GEO

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TRIM21 knockout mouse livers show enhanced antioxidant capacity and decreased compensatory proliferation

Project description:TRIM21 knockout mouse livers show enhanced antioxidant capacity and decreased compensatory proliferation

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Effect of Trim21 knockdown on MAPK and ERBB signaling pathways

Project description:To investigate Trim21 knockdown on the gene expression of downstream effectors of MAPK and ERBB pathways, we established HPAC cell lines with Trim21 knockdown.

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TRIM21 aggravates cardiac injury after myocardial infarction via promoting M1 macrophage polarization

Project description:Macrophage polarization followed by acute myocardial infarction (MI) is essential for the regulation of inflammation and scar formation. Tripartite motif-containing protein 21 (TRIM21), a member of E3 ubiquitin ligases, is a crucial mediator in the process of inflammation and heart failure. However, the potential roles of TRIM21 in modulating post-MI inflammation and macrophage polarization remain elusive. We detected that the levels of TRIM21 were significantly reduced in macrophages of WT mice after MI. In contrast, MI was ameliorated in TRIM21 knockout (TRIM21-/-) mice with improved cardiac remodeling, characterized by a marked decrease in mortality, increased wall thickness, and improved cardiac function in comparison with wild-type (WT) MI mice. Importantly, TRIM21 deficiency decreased the post-MI apoptosis and DNA damage in the hearts of mice, and the accumulation of M1 phenotype macrophages in infarcted hearts significantly decreased in TRIM21-/- mice compared with WT controls. Mechanistically, depletion of TRIM21 orchestrated the process of M1 macrophage polarization via a PI3K/Akt signaling pathway. Overall, these data reveal that TRIM21 drives the inflammatory response and cardiac remodeling after MI via stimulating M1 macrophage polarization through a PI3K/Akt signaling pathway.

2022-12-31 | GSE214696 | GEO

TRIM21 enhances bortezomib sensitivity in multiple myeloma by halting pro-survival autophagy

Project description:Bortezomib (bort) is an effective therapeutic agent for multiple myeloma (MM) patients; however, the majority of patients develop drug resistance. Autophagy, a highly conserved process that recycles cytosol or entire organelles via lysosomal activity, is essential for the survival, homeostasis and drug resistance in MM. Growing evidence has highlighted that E3 ligase tripartite motif-containing protein 21 (TRIM21) not only interacts with multiple autophagy regulators but also participates in drug resistance in various cancers. However, to date, the direct substrates and additional roles of TRIM21 in MM remain unexplored. In this study, we demonstrated that low TRIM21 expression is a factor for relapse in MM. TRIM21 knockdown (KD) made MM cells more resistant to bort, while TRIM21 overexpression (OE) resulted in increased MM sensitivity to bort. Proteomic and phospho-proteomic studies of TRIM21 KD MM cells showed that bort resistance was associated with increased oxidative stress and elevated pro-survival autophagy. Our results provided that TRIM21 KD MM cell lines induced pro-survival autophagy after bort treatment, and suppressing autophagy by 3-methyladenine treatment or by the short hairpin RNA of ATG5 restored bort sensitivity. Indeed, autophagy-related gene 5 (ATG5) expression was increased and decreased by TRIM21 KD and OE, respectively. TRIM21 affected autophagy by ubiquitinating ATG5 through K48 for proteasomal degradation. Importantly, we confirmed that TRIM21 could potentiate the anti-myeloma effect of bort through in vitro and in vivo experiments. Overall, our findings define the key role of TRIM21 in MM bort resistance and provide a foundation for a novel targeted therapeutic approaches.

2023-10-24 | PXD042004 | Pride

Transcriptome-wide analysis of TRIM21-mediated changes in gene expression after challenge with virus and antibody

Project description:We report that TRIM21 plays a crucial role in mediating antibody interference of adenovirus gene delivery and simultaneously initiates a transcriptional programme of immune genes.

2018-09-17 | GSE119119 | GEO

EPDR1 promotes PD-L1 expression and antitumor immune evasion by inhibiting TRIM21-dependent ubiquitylation if IKBKB.

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2024-06-29 | GSE250169 | GEO

TRIM21 innate immune detection of GBP1-positive Toxoplasma gondii is essential for host survival

Project description:Interferon gamma (IFN) is the major pro-inflammatory cytokine conferring resistance to the intracellular vacuolar pathogen Toxoplasma gondii. Autophagy along with immunity-related GTPases (IRGs), guanylate binding proteins (GBPs) and the E3 ubiquitin ligase TNF receptor-associated factor 6 (TRAF6) mediate clearance of Toxoplasma in IFN-stimulated cells. With the exception of inflammasomes, no host innate immune mediators impacting host survival have been identified at disrupted parasitophorous vacuoles. We show that IFN drives recruitment of the E3 ubiquitin ligase TRIM21 to GBP1-positive avirulent Toxoplasma vacuoles. This led to Lys63-linked ubiquitination of the vacuole and secretion of pro-inflammatory cytokines. GBPs were ubiquitinated during infection and TRIM21 controlled their expression levels and the efficient recruitment of GBP1 to the vacuole. TRIM21 deficiency led to an enhanced early replication of Toxoplasma without interfering with vacuolar disruption. TRIM21-/- mice were highly susceptible to Toxoplasma infection, exhibiting decreased levels of pro-inflammatory cytokines and higher parasite burden in the brain. This study identifies TRIM21 as a previously unknown modulator of Toxoplasma gondii resistance thereby extending host innate immune recognition of eukaryotic pathogens to include E3 ubiquitin ligases.

2018-03-12 | PXD003217 | Pride

MARC1 p.A165T variant is associated with decreased markers of liver injury and enhanced antioxidant capacity in autoimmune hepatitis.

Project description: Not available

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Dromedary Milk Protein Hydrolysates Show Enhanced Antioxidant and Functional Properties

Project description: Not available

| S-EPMC7416125 | biostudies-literature

PPDPF suppresses the development of hepatocellular carcinoma through TRIM21-mediated ubiquitination of RIPK1

Project description:Our study have shown that PPDPF promoted NF-κB activation through TRIM21-mediated K63-linked ubiquitination of RIPK1 in hepatocytes. Upon TNF-α stimulation, PPDPF enhances TRIM21/RIPK1 interaction and increases TRIM21-mediated K63-linked ubiquitination of RIPK1, which promotes NF-κB activation.To map the ubiquitination site of RIPK1 regulated by PPDPF, we performed MS analysis using control and RIPK1-overexpressing HEK293T cells with or without PPDPF overexpression

2023-02-21 | PXD040301 | iProX

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