RNF36 Blocking Peptide
- Known as:
- RNF36 Blocking Peptide
- Catalog number:
- 33r-8537
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- RNF36 Blocking Peptide
Ask about this productRelated genes to: RNF36 Blocking Peptide
- Gene:
- TRIM69 NIH gene
- Name:
- tripartite motif containing 69
- Previous symbol:
- RNF36
- Synonyms:
- Trif, TRIMLESS
- Chromosome:
- 15q15-q21
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-10
- Date modifiied:
- 2015-08-26
Related products to: RNF36 Blocking Peptide
Related articles to: RNF36 Blocking Peptide
- The dengue virus (DENV) can cause various clinical syndromes and organ damage, known as dengue fever, with the probability of developing severe dengue. However, the underlying mechanisms of host response against DENV infection remain unclear, and there is still no specific medicine for dengue fever. In the present study, we revealed the transcriptomic features of the host factor in patients with DENV infection and explored potential therapeutic medication. - Source: PubMed
Publication date: 2026/04/30
Liu ChengxinYu XinboChen JiafanZhong MingYe BeiWang KaiJiang YongLi GengZhan Shaofeng - The cytosolic sensor cyclic guanosine monophosphate-adenosine monophosphate (cGAMP) synthase (cGAS) is in charge of cytosolic DNA sensing and, as a result, the production of 2'3' cyclic GMP-AMP (cGAMP), which acts as a second messange molecule to activate the stimulator of interferon genes (STING) and the type I interferon (IFN-I) signalling pathway. We demonstrated that the E3 ubiquitin ligase enzyme TRIM69-induced ubiquitination of STING is necessary for cGAS-STING-mediated IFN-I production during antiviral innate immunity. A direct connection between TRIM69 and STING is essential for the ability of TRIM69 to activate the K63-linked ubiquitination of STING, which results in a significant increase in dimerization and downstream activation of TBK1. These findings suggest that TRIM69 is a novel, positive regulatory protein of the cytosolic DNA-sensing pathway, promoting the cGAS-STING signalling pathway. - Source: PubMed
Publication date: 2026/03/20
Chen ShixinYi LiXue MengzhouZheng Chunfu - Several proteins in the tripartite-motif (TRIM) family are associated with the development of systemic lupus erythematosus (SLE), but the role of TRIM69 in SLE is still poorly elaborated. - Source: PubMed
Publication date: 2026/02/20
Zhan JiahuanTu ChaofeiSu RiguLuo QingHuang ZikunLong DanLi Junming - Elevated sodium concentrations are commonly observed in tumors and sites of inflammation. Previous studies have shown that high salt levels modulate the phenotype and function of CD4 and CD8 T cells, regulatory T cells, and macrophages. In this study, we performed transcriptomic studies that revealed profound alterations in the neutrophil transcriptome upon high salt exposure, with changes that significantly exceeded those triggered by conventional agonists. By integrating transcriptomic data with functional assays, our findings suggest that high salt-induced neutrophil activation involves mitochondrial ROS production, which subsequently activates p38 MAPK and engages FOS-, Bruton's tyrosine kinase (BTK)-, and cyclooxygenase 2 (COX2)-dependent pathways. Remarkably, the plasticity of the neutrophil transcriptome in response to high salt was further evidenced by the upregulation of genes typically associated with other cell types, including semenogelin 1 (), intercellular adhesion molecule-4 (), tripartite motif69 (), amphiregulin (), oncostatin (), and transducer of ERBB2-1 (), suggesting a broader role for neutrophils in different biological processes beyond their participation in innate immunity. - Source: PubMed
Publication date: 2026/01/21
Mazzitelli IgnacioBleichmar LucíaRivelli FedericoFeijoo IngridAdamczyk AlanCabrerizo GonzaloErra Díaz FernandoGeffner Jorge - In the study, we investigated the effect of cryopreservation on the immune response of endometrial stromal cells (ESCs) to lipopolysaccharide (LPS). We exposed both frozen-thawed and untreated ESCs to LPS and measured cytokine levels as well as genes associated with the LPS-TLR4-cytokine signaling pathway. Results revealed that LPS induced significant upregulation of IL-1β, IL-6, IL-8, and TNF-α in vitro cultured untreated cells compared to frozen-thawed ones. Furthermore, mRNA levels related to the TRIF pathway, including TRAM, TRAF-6, and IRF-7, NF-κB, and JNK were significantly upregulated in untreated ESCs after LPS-stimulation but not in frozen-thawed cells. Moreover, transcription levels of TRIF signaling-related genes were notably lower in frozen-thawed cells. Additionally, TRIM69 overexpression rescued the cryopreservation-induced suppression of immune response. Overall, our findings suggest that cryopreservation attenuates the LPS-induced immune response in ESCs by inhibiting the TRIF pathway. - Source: PubMed
Publication date: 2025/12/23
Yang CuitingZhang YanWang ChunZhu LingxiZhang Ming