Trim35 Antibody - middle region (ARP34444_P050)
- Known as:
- Trim35 Antibody - middle region (ARP34444_P050)
- Catalog number:
- arp34444_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- Trim35 Antibody - middle region (ARP34444_P050)
Related genes to: Trim35 Antibody - middle region (ARP34444_P050)
- Gene:
- TRIM35 NIH gene
- Name:
- tripartite motif containing 35
- Previous symbol:
- -
- Synonyms:
- KIAA1098, MAIR, HLS5
- Chromosome:
- 8p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-11-21
- Date modifiied:
- 2014-11-19
Related products to: Trim35 Antibody - middle region (ARP34444_P050)
Related articles to: Trim35 Antibody - middle region (ARP34444_P050)
- Although patients with papillary thyroid cancer (PTC) generally have a favourable prognosis, they still face the possibility of recurrence after surgery. Identifying biomarkers related to PTC initiation and progression is crucial. The role and regulatory mechanisms of tripartite motif containing 35 (TRIM35) in PTC remain unclear. This study aimed to investigate the expression, biological functions, and underlying mechanisms of TRIM35 in PTC. - Source: PubMed
Publication date: 2026/04/28
Zhang LiubingPeng AipingQin Yue - Chronic hepatitis B (CHB) and non-alcoholic fatty liver disease (NAFLD) frequently coexist, and lipid metabolic dysregulation may represent a shared biological feature between these conditions. However, the molecular mechanisms linking these conditions remain poorly defined. Transcriptomic datasets of CHB and NAFLD were analyzed to identify differentially expressed genes, followed by weighted gene co-expression network analysis (WGCNA), functional enrichment, and machine-learning-based feature selection. Gene set variation analysis (GSVA) was performed to assess pathway activity, and experimental validation was conducted in an FFA-induced steatosis model using HepG2 cells. Shared genes and lipid metabolism-related modules common to both CHB and NAFLD were identified. Functional enrichment revealed pathways associated with lipid metabolism and cellular stress regulation. Machine-learning analysis highlighted TRIM35 and MPP1 as potential key genes, which were further validated in vitro as upregulated in steatotic conditions. This integrative approach advances understanding of shared lipid metabolic features between CHB and NAFLD and suggests potential candidate genes for future investigation in disease diagnosis and therapy. - Source: PubMed
Publication date: 2026/05/11
Wang Lihuan - Cardiovascular diseases (CVDs) remain one of the leading causes of death worldwide. Although the well-known risk factors include hypertension, hyperglycemia, dyslipidemia and obesity, the latest studies implicate involvement of pathological mechanisms at the molecular level. Various cellular processes, including oxidative stress, inflammatory response, mitochondrial dysfunction, and ferroptosis, are regarded as contributors to the initiation and progression of CVDs. Ubiquitination, a post-translational modification essential for the maintenance of protein homeostasis, influences the pathogenesis of CVD through regulating protein degradation, signal transduction and cellular functionality. The enzymes E1, E2 and several E3 ligases (e.g., TRAF6, TRIM21, TRIM35) participate in autophagy, inflammation and cardiac remodelling, while deubiquitinating enzymes (DUBs) (e.g., USP25, OTUB1) modulate cardiac function by stabilizing calcium pumps or regulating key signalling molecules. For example, ubiquitination of TRPC3 Ca channels prevents them from functioning closely with phospholipase C; excessive accumulation of TRPC3 lowers cardiac contractility. On the other hand, new protein degradation technologies like Proteolysis-Targeting Chimera (PROTAC) are promising for precise selective down-regulation of disease-related proteins. This study will systematically summarize the molecular mechanisms of ubiquitination in CVDs and its potential therapeutics to provide theoretical support for mechanistic research and the development of new targeted drugs. - Source: PubMed
Publication date: 2025/12/15
Wang YanfeiLiu XuesongHu YongLi HongfanLi ZhaoyuXu HuiCheng LuQiao QianYe XueruiZhang HaolingSong ZhijingWang WeiZhang Jingjing - Endometrial carcinoma (EC), recognized as the predominant gynecologic malignancy, is associated with substantial mortality rates. While chemotherapy serves as a critical component in adjuvant and primary treatments, existing pharmacological interventions demonstrate limited efficacy in significantly extending overall survival. Consequently, deciphering the molecular mechanisms driving EC pathogenesis is essential for developing innovative therapies. Existing evidence implicates TRIM35 in tumor proliferation, invasion, and metastatic processes across multiple cancers. To investigate TRIM35's role in EC, we performed integrated bioinformatics analysis followed by experimental validation via RT-qPCR and western blotting, which confirmed its significant downregulation in EC tissues. Subsequently, we transfected endometrial cancer cells with lentiviral plasmids overexpressing TRIM35 to investigate its Impact on cellular proliferation, cell cycle, invasion, and migration. We found that overexpressing TRIM35 significantly inhibited proliferation, invasion, and migration. Further research revealed that TRIM35 regulates the ubiquitination of EIF3E. Additionally, TRIM35 modulates the CDK4/Cyclin D1 signaling pathway, suppressing EC cell proliferation. Intriguingly, overexpressing EIF3E reversed the inhibitory effects of TRIM35 in EC cells. In conclusion, our study demonstrates that TRIM35 regulates the ubiquitination of EIF3E and inhibits the CDK4/Cyclin D1 signaling pathway, thereby suppressing the malignant proliferation of EC. These findings suggested that TRIM35 has potential as a therapeutic target for EC. - Source: PubMed
Publication date: 2025/12/20
Wang QiNing NingLi Yan - Hypoxia significantly influences the development of pulmonary hypertension (PH). However, the role of transfer RNA-derived small RNAs (tsRNAs) produced by nuclease cleavage on PH, particularly their impact on the proliferation of pulmonary artery endothelial cells (PAECs), remains unclear. - Source: PubMed
Publication date: 2025/12/05
Wang XuLi SongyueHou JianliCao ShukunZhang YibinZhang JingyaWang XinruSong XinyueXu YaQi JingXing YanZheng Xiaodong