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)
- Human adenovirus type 7 (HAdV-7) can cause severe pneumonia and sepsis in children, but the associated host epigenetic and immune alterations remain poorly defined. We profiled peripheral-blood DNA methylation in 11 children with HAdV-7-associated sepsis (6 survivors and 5 non-survivors) and 5 pediatric controls without clinically detectable HAdV-7 infection using reduced representation bisulfite sequencing. Differentially methylated genes were integrated with pediatric septic shock transcriptomic modules from GSE26440, and their cellular distribution and predicted regulatory effects were explored using the single-cell dataset GSE167363 and scTenifoldKnk. We identified 106 genes showing differential methylation across all three pairwise comparisons. Cross-cohort integration prioritized 19 candidate genes, among which TP53INP1 showed preferential expression in B cells in the external sepsis single-cell dataset. In silico perturbation of TP53INP1 was associated with changes in interferon-stimulated and antiviral genes, including TRIM22, IFI44L, and PARP14. These findings identify TP53INP1 as a hypothesis-generating candidate linking HAdV-7-associated whole-blood methylation changes with B-cell regulatory networks observed in an external sepsis dataset. Given the small discovery cohort and absence of experimental validation, the findings are exploratory and require confirmation in independent cohorts. - Source: PubMed
Publication date: 2026/09/17
Hu PeidanHuang BolunYang WenminZhang ChunminHuang JindaYang YiyuChen Feiyan - Despite the global burden of hepatitis E virus (HEV) infection, host-virus interactions underlying HEV pathogenesis and progression to chronicity remain incompletely understood. This study aimed to characterize the host transcriptomic response to infection with HEV variants harboring different host- and virus-derived insertions in the hypervariable region (HVR), with a focus on innate immune activation. - Source: PubMed
Publication date: 2026/09/17
Schlienkamp SarahNocke Maximilian KUlrich Rainer GKinast VolkerSteinmann EikeTodt Daniel - Clear cell renal cell carcinoma (ccRCC) represents one of the most prevalent malignancies worldwide, characterized by high incidence and mortality rates. It is characterized by mitochondrial dysfunction with enhanced Warburg effect. In this study, we identify the sortilin-related receptor 1 (SORL1) as a regulator of ccRCC progression and a potential molecular target for oxidative phosphorylation inhibition. The present evidence demonstrates that SORL1 promotes the ubiquitin-mediated degradation of C-MYC via TRIM22, which is associated with the downregulation of ACO2 and IDH2 and a consequent suppression of oxidative phosphorylation capacity. Molecular investigations further indicated that Cefoperazone could bind to SORL1 and increase its protein level, exerting the SORL1-triggering function. Targeting delivery Cefoperazone exhibits unexpected anti-tumor performances in ccRCC. Collectively, our findings establish SORL1 as a tumor suppressor in ccRCC and highlight its potential as a therapeutic target in advancing ccRCC clinical treatment strategies. - Source: PubMed
Publication date: 2026/09/04
Wang KeyiSong WeiBai QiShen ShaozeLu XiaoSu ChenxuanYang ShiWang YidiXia YuZan RuiJiang ShuaiGuo Jianming - Ulcerative colitis (UC) is a chronic, relapsing inflammatory disorder of the colonic mucosa. Although colonoscopy remains the diagnostic cornerstone for UC, its invasive nature highlights the need for additional biomarkers. This study used differential expression analysis, weighted gene co-expression network analysis (WGCNA), and machine-learning algorithms to identify three key platelet-related genes (PRGs)-TRIM22, TIMP1, and RAC2-that are involved in UC development. Immune cell analysis and single-cell analyses indicated that the expression of these key genes was significantly correlated with macrophages, neutrophils, and mast cells. Moreover, these key PRGs were mainly involved in pathways related to UC, such as chemokine signaling and leukocyte transendothelial migration. The expression levels of the key PRGs were further validated in independent datasets, dextran sulfate sodium (DSS)-induced colitis tissues, and peripheral blood mononuclear cells (PBMC) samples from UC patients. Collectively, these findings support a platelet-related three-gene signature with potential diagnostic and biological relevance in UC. - Source: PubMed
Publication date: 2026/08/25
Huang JinDai YingLu ShuangshuangLi XueSun RuihongHuang BenMa Chunmei - 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