TRIM22 293T Cell Transient Overexpression Lysate(Denatured)
- Known as:
- TRIM22 293T Cell Transient Overexpression Lysate(Denatured)
- Catalog number:
- H00010346-T01
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- TRIM22 293T Cell Transient Overexpression Lysate(Denatured)
Related genes to: TRIM22 293T Cell Transient Overexpression Lysate(Denatured)
- Gene:
- TRIM22 NIH gene
- Name:
- tripartite motif containing 22
- Previous symbol:
- -
- Synonyms:
- STAF50, GPSTAF50, RNF94
- Chromosome:
- 11p15.4
- Locus Type:
- gene with protein product
- Date approved:
- 2001-08-10
- Date modifiied:
- 2016-10-05
Related products to: TRIM22 293T Cell Transient Overexpression Lysate(Denatured)
Related articles to: TRIM22 293T Cell Transient Overexpression Lysate(Denatured)
- This study investigates the functional role of DNAJB9 in the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP). Using quantitative proteomics alongside human tissue analysis and murine models, we found that DNAJB9 is significantly upregulated in CRSwNP nasal epithelium and closely mirrors epithelial-mesenchymal transition (EMT) progression. Functional assays in human epithelial cells demonstrated that DNAJB9 actively drives the EMT phenotype. Mechanistically, DNAJB9 interacts with and stabilizes the E3 ubiquitin ligase TRIM22 by inhibiting its autoubiquitination. This stabilized TRIM22 targets IκBα for proteasomal degradation, leading to constitutive NF-κB pathway activation and subsequent EMT. Ultimately, DNAJB9 acts as an essential driver of tissue remodeling in CRSwNP. These findings highlight the broader clinical significance of the DNAJB9/TRIM22/NF-κB signaling axis, presenting it as a promising therapeutic target for inhibiting nasal polyp formation and associated remodeling. - Source: PubMed
Publication date: 2026/07/16
Zhang ZhiqiangHuang XinyuTu JunhaoLiu MengyuanWu YingZhang XuZhang YunYang Chunping - Multiple programmed cell death (PCD) modalities, including apoptosis, autophagy, and ferroptosis, are closely implicated in spontaneous preterm birth (SPTB). Mitochondria serve as central regulators of various PCD pathways, playing a critical role in cellular stress responses and homeostasis. However, comprehensive studies integrating mitochondria-localized protein-encoding genes and PCD-related genes to explore the molecular mechanisms underlying SPTB remain limited. - Source: PubMed
Publication date: 2026/07/20
Zuo LuguangHuai QingsongZhang MingmingLiu XinShang Xiaoling - Interleukins (ILs) are pleiotropic mediators of immune signaling and represent promising targets for antiviral intervention. Among them, IL-19 is upregulated in response to viral infections, yet its functional significance and mechanistic basis have been poorly defined. This study identifies an unforeseen antiviral activity of IL-19. Mechanistically, we demonstrate that IL-19 signals through the IL-20RB receptor to drive STAT3 phosphorylation, and this activated IL-20RB/STAT3 pathway then induces TRIM22 expression, culminating in enhanced IFN-λ secretion and the direct suppression of viral replication. Importantly, despite significantly curtailing HSV-1 replication in murine brain and lung tissues, IL-19 administration failed to confer a survival benefit, an effect attributable to aggravated pulmonary inflammation. These findings clarify IL-19 as a dual-function cytokine with both protective antiviral and detrimental proinflammatory properties, illustrating the intricate immunomodulatory functions of cytokines during viral infections. - Source: PubMed
Zhang XinyuWu FanHu XinruSong ZiwenDeng LishaLiao YuShi MinjuanHan ZirongWang LijieSun Caijun - This study aimed to identify ubiquitination-related diagnostic biomarkers in diabetic nephropathy (DN), explore their molecular mechanisms and candidate therapeutic agents, and further validate their expression and functions through experiments conducted in vivo and in vitro. The GSE30122 dataset from the GEO database was used to screen for differentially expressed genes (DEGs). Ubiquitination-related genes (URGs) were derived from the GSEA database. Weighted gene coexpression network analysis (WGCNA) was applied for the identification of ubiquitination-associated gene modules. Least absolute shrinkage and selection operator (LASSO) logistic regression and support vector machine-recursive feature elimination (SVM-RFE) algorithms were used to screen for ubiquitination-related diagnostic biomarkers in DN. A nomogram diagnostic model was established. ssGSEA was applied to analyze how these biomarkers are related to immune cell types and immune processes. Different ubiquitination-related DN subtypes were identified using consensus cluster analysis. The single-cell dataset GSE195460 was used to explore the cellular distribution of diagnostic biomarkers. Drug prediction and molecular docking were conducted to identify promising therapeutic agents. In vivo (mouse and human DN tissues) and in vitro (NLK-overexpressing podocytes) validation was conducted. Five ubiquitination-related diagnostic biomarkers (TRIM22, RCN1, ZNF204P, LPGAT1, and NLK) were identified, and the nomogram model showed good diagnostic efficiency. Immune-related analysis revealed that these diagnostic biomarkers were significantly associated with immune cells and immune processes. DN samples were clustered into three ubiquitination-related subtypes, with the high-expression subtype exhibiting lower immune infiltration. The molecular docking results indicated that quercetin had favorable binding energies with TRIM22, LPGAT1, and NLK and that resveratrol had good binding energy with RCN1. In vivo validation demonstrated that TRIM22, RCN1, and LPGAT1 were upregulated, whereas NLK was downregulated in the renal tissues of both humans and mice with DN. In vitro experiments confirmed that NLK overexpression ameliorated high glucose-induced podocyte injury and apoptosis by increasing the expression of podocyte markers (podocin and WT1) and Bcl-2 (an antiapoptotic protein) while concurrently reducing the expression of Bax and caspase-1 (proapoptotic proteins). TRIM22, RCN1, ZNF204P, LPGAT1, and NLK are potential diagnostic biomarkers for DN, and the constructed nomogram model has good diagnostic performance. Diagnostic biomarkers are strongly associated with immune cells and immune processes. Quercetin and resveratrol are potential therapeutic agents targeting these biomarkers. NLK may play a protective role in DN by alleviating podocyte injury and apoptosis. - Source: PubMed
Dong TingHu MiaoYu HaiboZhou LingQiao Qing - Ankylosing Spondylitis (AS) is a chronic inflammatory autoimmune rheumatic disease that primarily affects the spine and sacroiliac joints. This study aimed to investigate the expression levels of immune response-related genes, including , , , , , , and , as well as the serum levels of CXCL10 and SIRPA proteins in patients with AS. In addition, the potential diagnostic performance of these molecular and serum biomarkers in distinguishing patients with AS from healthy controls was evaluated. A total of 45 patients with AS and 44 healthy controls were included in the study. Immune-related gene expression levels were analyzed using RT-PCR. In addition, serum CXCL10 and SIRPA protein levels were evaluated using ELISA. The expression levels of , , , , and were significantly increased in patients with AS compared to healthy controls ( < 0.05). In contrast, no significant differences were detected in the expression levels of and . In the ROC analysis, the highest diagnostic performance was obtained for (AUC = 0.741), (AUC = 0.720), and (AUC = 0.722). Serum CXCL10 and SIRPA levels were not significantly different between the groups. In AS, genes particularly associated with NF-κB and interferon signaling pathways (, , , , and ) were found to be significantly altered, and these genes may serve as potential molecular biomarkers for AS. In contrast, the diagnostic power of serum protein biomarkers is limited. These findings indicate that the potential of these genes as biomarkers for AS pathogenesis should be further supported by advanced studies evaluating their expression levels. - Source: PubMed
Publication date: 2026/06/27
Dogan Sevil CeyhanAgbektas TugbaAtas MertKabak GoncaTas AycaSilig Yavuz