TRIM22 Over-expression Lysate Product
- Known as:
- TRIM22 Over-expression Lysate Product
- Catalog number:
- GWB-FA53DE
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- TRIM22 Over-expression Lysate Product
Related genes to: TRIM22 Over-expression Lysate Product
- 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 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: TRIM22 Over-expression Lysate Product
- Lysine acetyltransferase 2A (KAT2A) is a transcriptional coactivator and a member of the Histone Acetyltransferase (HAT) family. While altered KAT2A activity has been implicated in various cancers, its role in bladder cancer (BLCA) remains poorly understood. Post-translational modifications (PTMs), such as O-GlcNAcylation, play a critical role in cancer biology. In this study, we investigated the impact of O-GlcNAcylation on KAT2A stability and its oncogenic potential in BLCA. We analyzed 96 paired BLCA and normal tissue samples using quantitative real-time PCR (qPCR) and immunohistochemistry to assess KAT2A expression. Functional assays, including siRNA-mediated knockdown, co-immunoprecipitation (co-IP), ubiquitination, and chromatin immunoprecipitation (ChIP), were conducted in BLCA cell lines and xenograft models to understand KAT2A O-GlcNAcylation mechanisms. We found that KAT2A expression was significantly increased in BLCA tissues. O-GlcNAcylation at serine 583 (S583) stabilized KAT2A by inhibiting TRIM22-mediated ubiquitination. Hyper-O-GlcNAcylation increased H3K9 acetylation and upregulated oncogenes like TGFB1, E2F1, and GPX4, promoting cell proliferation and tumor growth. Mutation of S583 destabilized KAT2A, impaired H3K9 acetylation, and suppressed oncogene expression. Our results highlight the pivotal role of KAT2A in BLCA and demonstrate that O-GlcNAcylation at S583 is a crucial regulatory mechanism driving tumor progression. Targeting KAT2A O-GlcNAcylation may provide a promising therapeutic strategy for BLCA patients. - Source: PubMed
Publication date: 2026/05/11
Yang WenjieJin ZhaohengLi ZiyiXu WeifengLi YingjiePeng YueqiangDong JieMa LinJi Zhigang - Glioblastoma (GBM) is one of the most aggressive brain tumors with a poor prognosis despite current treatment modalities. This study aimed to identify genes whose high expression is paradoxically associated with both poor survival and enhanced immune activity, as potential targets for combination chemotherapeutic and immunotherapeutic strategies. - Source: PubMed
Publication date: 2026/04/27
Han Myung-HoonNoh Yung-KyunKim HyunkeeKim Kyu ShikKim Dong-HoonJung Un SukLee Kyung SukKwon Mi JungChae Seoung WanMin Kyueng-Whan - Acquired resistance limits the therapeutic efficacy of KRAS-MAPK inhibitors in pancreatic ductal adenocarcinoma (PDAC). As transcriptional plasticity and epithelial-to-mesenchymal transition (EMT) have been implicated in resistance, we sought to study the molecular mechanisms driving these changes to uncover actionable vulnerabilities. Sustained KRAS-MAPK inhibition induced interferon and NF-κB signaling and promoted cell state change mimicking an EMT state associated with drug resistance. Network analysis identified the interferon-inducible E3 ubiquitin ligase TRIM22 as a central regulator of this response. Mechanistically, TRIM22 promoted proteasomal degradation of IκBα, resulting in sustained NF-κB and EMT program activation that coincided with a basal-like transcriptional cell state. TRIM22 expression was driven by IRF1 and IRF9 following relief of ERK-mediated transcriptional repression during pathway inhibition. EMT induction was accompanied by marked upregulation of TROP2 (TACSTD2), an NF-κB target gene enriched in basal-like PDAC cell states. Combining TROP2-directed antibody-drug conjugate sacituzumab govitecan with KRAS or ERK inhibitors significantly suppressed PDAC tumor growth in xenograft models. Overall, prolonged KRAS-MAPK inhibition activates an interferon-TRIM22-NF-κB axis that drives EMT and therapeutic resistance in PDAC, while revealing TROP2 as a clinically actionable vulnerability to overcome acquired resistance. - Source: PubMed
Publication date: 2026/04/20
Bulle AshenafiChen YaliLi HuapingChen Timothy Hung-PoKhawar Iftikhar AliLi LinWang YuLiu PengSomani Vikas KumarKurupi RichardGeng YutongPereye Ofejiro BlessingBansod SapanaLe Son BRuzinova Marianna BTran David DLim Kian-Huat - Liver cirrhosis(LC) represents the end stage of chronic liver disease, yet reliable molecular markers remain limited. This study aimed to uncover potential diagnostic biomarkers and therapeutic targets for LC. - Source: PubMed
Publication date: 2026/03/14
Zhang KangChen TingJia ZhangyuZhao JunxiaHuang Na - - Source: PubMed
Publication date: 2026/02/28
Liu JinghongZhang JianboChen QunxiangQing WeijiaPeng YongchunHe ZhijingZhou XiPi HuifengLi BoLin QingyunLiu JunxinZhang FanZhang ShengFan Tengfei