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

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

PROVIDER: PRJNA488224 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7761110.fastq.gz	Fastqsanger.gz
	SRR7761120.fastq.gz	Fastqsanger.gz
	SRR7761130.fastq.gz	Fastqsanger.gz
	SRR7761140.fastq.gz	Fastqsanger.gz
	SRR7761111.fastq.gz	Fastqsanger.gz

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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

Neutralizing Antibody Mediated Protection Against Mucosal Simian-Human Immunodeficiency Virus Challenge Includes Systemic Clearance of Distal Virus

Project description:The purpose of this study was to investigate the anatomic sites and mechanisms of antibody-mediated protection. In particular, to determine whether bNAbs completely block virus at the local portal of entry following mucosal virus challenge.

2016-09-01 | GSE83702 | GEO

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.

2023-08-08 | GSE208568 | GEO

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

Pa01c cells stable expressing a scramble or shRNA against TRIM21

Project description:We make Pa01c cells stable expressing a scramble or shRNA against TRIM21 and performed bulk scRNASeq to assess transcriptomic changes Pa01c cells

2024-11-21 | GSE207852 | 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

TRIM21-mediated protein depletion recapitulates mutant gene phenotype in early mouse embryos

Project description:It is often desirable to be able to regulate or impair the expression of specific genes to study early developmental events in the mammalian embryo. While DNA and RNA methods are routine, methods using proteins are still in their infancy. When proteins in the cell encounter a specific antibody and the ubiquitin-protein ligase TRIM21, a ternary complex forms with the target protein, leading to its rapid and acute degradation – hence the name ‘Trim-Away'. However, there are many unknowns in this new endeavour. First and foremost, the extent to which endogenous proteins can be depleted depends on their amount in relation to the amount of exogenous antibody, which is limited by the microinjection procedure. Secondly, the depletion of the protein must be sustained over days. Using mass spectrometry and the iBAQ algorithm, we estimate the amount of proteins found in preimplantation mouse embryos. Most of these amounts are tractable with the microinjection method presented here, which supplies 10E-4 picomoles of antibody contained in 100 picolitres, before incurring toxic effects on mouse development. Building on these data, we demonstrate the feasibility of protein knock-down for a gene which is essential in the preimplantation mouse embryo, namely TEA domain family member 4 (Tead4). Knock-down persists long enough to result in a phenotype which is entirely consistent with that of the null mutation and the RNA interference: significantly reduced mRNA expression of TEAD4 target genes Cdx2 and Gata3, failure of CDX2 nuclear translocation and the embryo’s inability to implant. We conclude that at least for a time window of 3-4 days of preimplantation development, protein depletion is on the rise as a valid alternative to DNA and RNA methods.

2019-09-11 | PXD012613 | Pride

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

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

2021-04-14 | GSE164369 | GEO

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 |

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

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