RORE EMSA Probe Set
- Known as:
- RORE EMSA Probe Set
- Catalog number:
- AY1395P
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- RORE EMSA Probe Set
Related genes to: RORE EMSA Probe Set
- Gene:
- TRIM38 NIH gene
- Name:
- tripartite motif containing 38
- Previous symbol:
- RNF15
- Synonyms:
- RORET
- Chromosome:
- 6p22.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-03-06
- Date modifiied:
- 2016-10-05
Related products to: RORE EMSA Probe Set
(+) Control probe (DNA), biotinylated(+) Control probe (RNA), biotinylated(-) Control probe (DNA), biotinylated(-) Control probe (RNA), biotinylated0.2 mm, 30 cm Spacer Set
0.2 mm, 30 cm Spacer Set0.35 mm, 30 cm Spacer Set
0.35 mm, 30 cm Spacer Set0.5 mm, 30 cm Spacer Set
0.5 mm, 30 cm Spacer Set0.75 mm Dual Gel Cast Set
0.75 mm Dual Gel Cast Set0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
Related articles to: RORE EMSA Probe Set
- Glioma constitutes approximately 50% of primary brain tumors. This study aimed to analyze the mechanism by which TRIM38 contributes to the progression of glioma. - Source: PubMed
Yang PengxiangLi Huiyong - Fibroblast-like synoviocytes (FLS) in rheumatoid arthritis (RA) synovium acquire a unique aggressive phenotype and produce cytokines that perpetuate inflammation and proteases that contribute to cartilage destruction. Actin-bundling protein Fascin-1 (FSCN1) is involved in FLS migration and invasion, but its role and mechanism in FLS phenotypic activation remain unclear. - Source: PubMed
Publication date: 2026/08/17
Chen LiangyuWu JunfengZhou TaoZou ZilinCheng QinweiChen DalinLi HonghaoYang PanpanYang ChengliangWang HongLi Kai - This article explored the role of TRIM38 in ferroptosis in heart failure (HF) and its underlying mechanisms. Methodologically, serum TRIM38, IRAK1 and TRAF6 proteins from HF patients were detected by Western blot. In an in vitro study, an HF cell model was established by inducing H9c2 cells with doxorubicin. Through a series of logical experiments, the effects of TRIM38 and IRAK1 on oxidative stress and ferroptosis in the HF cell model, and the underlying mechanisms, were researched. Notably, serum TRIM38 was decreased in HF patients, while IRAK1 and TRAF6 were increased. In the HF cell model, TRIM38 silencing enhanced oxidative stress and ferroptosis, which were reversed by ferrostatin-1, a ferroptosis inhibitor. TRIM38 caused ubiquitination degradation of IRAK1 protein. TRIM38 overexpression suppressed oxidative stress, ferroptosis, and the TRAF6-p38 MAPK pathway activity in the HF cell model, but this suppression was abrogated by IRAK1 overexpression. TRAF6 could activate p38 MAPK in the HF cell model. TRAF6 silencing or inhibiting p38 MAPK reversed the promotion of TRIM38 silencing on oxidative stress and ferroptosis in the HF cell model. Overall, TRIM38 might alleviate ferroptosis in HF by inactivating the TRAF6-p38 MAPK pathway via ubiquitinating IRAK1, suggesting TRIM38 as a potential therapeutic target for HF. - Source: PubMed
Liu YunJia HaiyuZhang YongBao Qiuhong - Circular RNAs (circRNAs) have been implicated in various cardiovascular diseases and hold promise as diagnostic biomarkers and therapeutic targets. However, the roles and mechanisms of circRNAs in coronary artery disease (CAD) and its severe complication, acute myocardial infarction (AMI), remain unclear. CircRNA sequencing, fluorescence in situ hybridization, and quantitative PCR were used to assess circTMCC1 expression in human coronary artery segments, peripheral blood mononuclear cells (PBMCs) from CAD patients, M1 macrophages, and an AMI mouse model. Multiple analytical methods were employed to investigate the predictive value of circTMCC1 for quantitative flow ratio (QFR) measurements. In vitro, we employed plasmid overexpression, small interfering RNA transfection, flow cytometry, immunofluorescence, reactive oxygen species (ROS), and mitochondrial membrane potential assays. In vivo, Masson's trichrome, hematoxylin and eosin staining, and immunohistochemistry were performed. Mechanistic investigations included bioinformatics, RNA pull-down, RNA immunoprecipitation, co-immunoprecipitation, western blotting, and immunofluorescence. CircTMCC1 was significantly upregulated in CAD patients (p < 0.001) and associated with poor prognosis in AMI mouse models. CircTMCC1 was highly expressed in M1 macrophages (p < 0.001), and silencing its expression reduced M1 polarization, improved cardiac function after infarction, and regulated mitochondrial autophagy. Mechanistically, circTMCC1 facilitates the interaction between annexin A1 and the E3 ligase TRIM38, leading to annexin A1 degradation. Additionally, the AMPK/mTOR signaling pathway was identified as a downstream target of circTMCC1. These findings suggest that circTMCC1 may serve as a promising diagnostic biomarker and therapeutic target for CAD and AMI, potentially improving prognosis. - Source: PubMed
Publication date: 2026/07/06
Ren MengmengHe ShuDuan MengyangChi BoyuChen ZhiyuanZhao ZhenyuCiren ZhonggaQiangba YangzongFu YahongWang GaochaoYuan LiangAn FenghuiJia Enzhi - Circadian Locomotor Output Cycles Kaput (CLOCK) is a core circadian gene encoding a transcription factor essential for maintaining physiological rhythms, and has more recently been implicated in cancer biology. In this study, we uncover an unrecognized tumor-suppressive role of CLOCK in nasopharyngeal carcinoma (NPC). Mechanistically, CLOCK directly activates NBR1 transcription, leading to the stabilization of p62/SQSTM1 and the co-assembly of NBR1-p62 condensates via liquid-liquid phase separation (LLPS). These condensates serve as scaffolds for the recruitment of the E3 ubiquitin ligase TRIM38, which mediates the ubiquitination and proteasomal degradation of TAK1-binding protein 2 (TAB2), thereby attenuating NF-κB signaling. Functionally, this axis suppresses NPC cell proliferation and migration. Our findings reveal a novel CLOCK-NBR1/p62-TRIM38-TAB2 pathway that links circadian gene to LLPS-driven tumor suppression in NPC, providing new insights into the role of circadian genes in cancer biology and pointing to a potential therapeutic target for this malignancy. - Source: PubMed
Publication date: 2026/06/10
Rashed NasotZhu YaQuan JingLi ZhengjiangZeng PaiLi HongdeLiu WenbinZeng XiLuo Xiangjian