TRIM3 Over-expression Lysate Product
- Known as:
- TRIM3 Over-expression Lysate Product
- Catalog number:
- GWB-578BEE
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- TRIM3 Over-expression Lysate Product
Related genes to: TRIM3 Over-expression Lysate Product
- Gene:
- TRIM3 NIH gene
- Name:
- tripartite motif containing 3
- Previous symbol:
- RNF22
- Synonyms:
- HAC1, BERP, RNF97
- Chromosome:
- 11p15.4
- Locus Type:
- gene with protein product
- Date approved:
- 2000-07-31
- Date modifiied:
- 2016-10-05
Related products to: TRIM3 Over-expression Lysate Product
(META) Human Metapneumovirus Type 16 (A1) Lysate(META) Human Metapneumovirus Type 18 (B2) Lysate(META) Human Metapneumovirus Type 20 (A2) Lysate(META) Human Metapneumovirus Type 27 (A2) Lysate(META) Human Metapneumovirus Type 3 (B1) Lysate(META) Human Metapneumovirus Type 4 (B2) Lysate(META) Human Metapneumovirus Type 5 (B1) Lysate(META) Human Metapneumovirus Type 8 (B2) Lysate(META) Human Metapneumovirus Type 9 (A1) Lysate0 day neonate eyeball cDNA. RIKEN full-length enriched library. clone E130107M17 product hypothetical protein. full insert seque - N_A Polyclonal0 day neonate head cDNA. RIKEN full-length enriched library. clone 4831434J02 product nuclear factor of activated T-cells. cytop - N_A Polyclonal0 day neonate head cDNA. RIKEN full-length enriched library. clone 4832421E02 product myocyte enhancer factor 2C. full insert se - N_A Polyclonal1,2,3,4-Tetrahydro-1,2-dimethyl-4,6-isoquinolinediol
(Major Product) CAS: 102830-16-0 Formula: C11H15NO21,2,3,4-tetrahydro-1,2-dimethyl-4,8-isoquinolinediol
(Minor Product) CAS: 102830-20-6 Formula: C11H15NO210 days embryo whole body cDNA. RIKEN full-length enriched library. clone 2610510L15 product poly(A)-specific ribonuclease (dead - N_A Polyclonal Related articles to: TRIM3 Over-expression Lysate Product
- Pediatric T-cell acute lymphoblastic leukemia (T-ALL) remains a therapeutic challenge, with approximately 20% of patients experiencing relapse due to a limited understanding of molecular drivers [...]. - Source: PubMed
Publication date: 2026/04/22
Sun YuXu YuhaoLu Chao - TRIM-NHL proteins, a subfamily of Tripartite Motif (TRIM) family proteins, are characterized by the presence of NHL structures in their C-terminal domains. In humans, this subfamily mainly includes TRIM2, TRIM3, TRIM32, TRIM71, and the recently discovered TRIM56 protein. The C-terminal domains of these five proteins exhibit varying degrees of difference. Increasing evidence indicates that TRIM proteins are involved in numerous physiological and pathological processes related to life and health, and TRIM71 is no exception. In this article, we introduce the functional and structural characteristics of TRIM family proteins. We mainly discuss the known functions and related specific structures of the TRIM71 protein in the TRIM-NHL subfamily, as well as the exploration of its druggability. We also summarize and organize its physiological functions and biological processes in disease regulation. - Source: PubMed
Publication date: 2026/05/12
Gan Qi-FengHan Zi-XvZheng Zu-Guo - Our objective was to investigate TRIM3 expression and its role in the immune microenvironment of non-small-cell lung cancer (NSCLC). - Source: PubMed
Publication date: 2026/03/23
Jiang WenfaChen Shuchen - Interferon-beta (IFN-β) has potent antitumor activity, but its clinical therapeutic potential is undermined by intrinsic negative feedback loops that suppress IFN-β production. However, the feedback mechanisms regulating IFN-β homeostasis in non-small cell lung cancer (NSCLC) remain unclear. We found that tripartite motif containing 3 (TRIM3) promotes the transcription and mRNA expression of IFNB1. Conversely, excessive IFN-β inhibits expression of TRIM3, creating their reciprocal feedback loop. Mass spectrometry revealed that toll-like receptor 3 (TLR3), a key sensor that triggers IFN-β production, is the interacting partner of TRIM3. Following the elucidation of the interactive mode between TRIM3 and TLR3, we found that activation of the TRIM3/TLR3 axis induced IFN-β secretion and overrode the feedback inhibition. Sustained IFN-β secretion subsequently inhibits NSCLC cell proliferation and reprograms the tumor microenvironment by increasing the infiltration levels of CD4 T cells, M1 macrophages and NK cells. Our findings revealed a reciprocal negative feedback loop in the regulation of IFN-β signaling, highlighting the role of the TRIM3/TLR3 axis in the suppression of NSCLC progression and offering a promising strategy to suppress tumor growth and enhance immunotherapy efficacy in NSCLC. - Source: PubMed
Publication date: 2026/01/16
Xu JianyuHu QianfangZhu YingLiu QianWang FengYu YanxiaWang WenjuanDing Xinyuan - As a leading cause of disability worldwide, osteoarthritis (OA) progressively degrades articular cartilage. The incomplete understanding of OA's molecular mechanisms hinders development of disease-modifying treatments. - Source: PubMed
Publication date: 2025/12/23
Ou HuashuangLi BaichuanLiang HaiboDeng HaiquanZhang LeiLan MindongCui XiangrongLi ShuzhenSun Jianchao