Mouse monoclonal to SPOP , Isotype IgG2a, Host Mouse, Clone 3E2
- Known as:
- Mouse mab SPOP , Isotype IgG2a, Host Mouse, Clone 3E2
- Catalog number:
- YF-MA16346
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Abfron
- Gene target:
- Mouse monoclonal SPOP Isotype IgG2a Host Clone 3E2
Related genes to: Mouse monoclonal to SPOP , Isotype IgG2a, Host Mouse, Clone 3E2
- Gene:
- SPOP NIH gene
- Name:
- speckle type BTB/POZ protein
- Previous symbol:
- -
- Synonyms:
- TEF2, BTBD32
- Chromosome:
- 17q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-07
- Date modifiied:
- 2016-02-10
Related products to: Mouse monoclonal to SPOP , Isotype IgG2a, Host Mouse, Clone 3E2
Related articles to: Mouse monoclonal to SPOP , Isotype IgG2a, Host Mouse, Clone 3E2
- Mutations in the speckle-type POZ (SPOP) gene are frequently identified in prostate cancer (PC); yet, prognostic implications for affected patients remain unclear. Limited consensus exists regarding tailored treatments for SPOP-mutant (SPOPmut) PC. - Source: PubMed
Publication date: 2024/05/03
Pedrani MartinoSalfi GiuseppeMerler SaraTesti IreneCani MassimilianoTurco FabioTrevisi ElenaTortola LuigiTreglia GiorgioDi Tanna Gian LucaVogl UrsulaGillessen SilkeTheurillat Jean-PhilippePereira Mestre Ricardo - The metastasis and aggressive nature of prostate cancer (PCa) has become a major malignancy related threat that concerns men's health. The efficacy of immune monotherapy against PCa is questionable due to its lymphocyte-suppressive nature. - Source: PubMed
Publication date: 2024/04/20
Wan LilinFan YunxiaWu TiangeLiu YifanZhang RuixinChen SaisaiZhao ChengguiXue Yifeng - Refractoriness to surgical resection and chemotherapy makes intrahepatic cholangiocarcinoma (ICC) a fatal cancer of the digestive system with high mortality and poor prognosis. Important function invests circRNAs with tremendous potential in biomarkers and therapeutic targets. Nevertheless, it is still unknown how circRNAs contribute to the evolution of ICC. - Source: PubMed
Publication date: 2024/04/20
Li JingXu XiaohongXu KaihaoZhou XueliangWu KunpengYao YuanLiu ZaoquChen ChenWang LingSun ZhenqiangJiao DechaoHan Xinwei - Accumulating evidence demonstrates that the activity regulation of ELK3, a member of the E26 transformation-specific oncogene family, is critical to regulating cell proliferation, migration, and survival in human cancers. However, the molecular mechanisms of how ELK3 induces chemoresistance in prostate cancer (PCa) have not been elucidated. In this study, we found that SPOP and ELK3 are an interacting partner. The interaction between SPOP and ELK3 resulted in increased ELK3 ubiquitination and destruction, assisted by checkpoint kinase-mediated ELK3 phosphorylation. Notably, the modulation of SPOP-mediated ELK3 protein stability affected the c-Fos-induced cell proliferation and invasion of PCa cells. The clinical involvement of the SPOP-ELK3 axis in PCa development was confirmed by an immunohistochemical assay on 123 PCa tissues, with an inverse correlation between increased ELK3 and decreased SPOP being present in ~80% of the specimens. This observation was supported by immunohistochemistry analysis using a SPOP-mutant PCa specimen. Finally, docetaxel treatment induced cell death by activating checkpoint kinase- and SPOP-mediated ELK3 degradation, while SPOP-depleted or SPOP-mutated PCa cells showed cell death resistance. Notably, this observation was correlated with the protein levels of ELK3. Taken together, our study reveals the precise mechanism of SPOP-mediated degradation of ELK3 and provides evidence that SPOP mutations contribute to docetaxel resistance in PCa. - Source: PubMed
Publication date: 2024/04/17
Lee Cheol-JungLee HeejungKim Seo ReeNam Soo-BinLee Ga-EunYang Kyeong EunLee Guk JinChun Sang HoonKang Han ChangLee Joo YoungLee Hye SukCho Sung-JunCho Yong-Yeon - Glioblastoma (GBM) exhibits profound metabolic plasticity for survival and therapeutic resistance, while the underlying mechanisms remain unclear. Here, we show that GBM stem cells (GSCs) reprogram the epigenetic landscape by producing substantial amounts of phosphocreatine (PCr). This production is attributed to the elevated transcription of brain-type creatine kinase (CKB), mediated by Zinc finger E-box binding homeobox 1 (ZEB1). PCr inhibits the poly-ubiquitination of the chromatin regulator bromodomain containing protein 2 (BRD2) by outcompeting the E3 ubiquitin ligase SPOP for BRD2 binding. Pharmacological disruption of PCr biosynthesis by cyclocreatine leads to BRD2 degradation and a decrease in its targets' transcription, which inhibits chromosome segregation and cell proliferation. Notably, cyclocreatine treatment significantly impedes tumor growth and sensitizes tumors to a BRD2 inhibitor in mouse GBM models without detectable side effects. These findings highlight that high production of PCr is a druggable metabolic feature of GBM and a promising therapeutic target for GBM treatment. - Source: PubMed
Publication date: 2024/04/02
Chen LishuQi QinghuiJiang XiaoqingWu JinLi YuanyuanLiu ZhaodanCai YanRan HaowenZhang SongyangZhang ChengWu HuiranCao ShuailiangMi LanjuanXiao DakeHuang HaohaoJiang ShuaiWu JiaqiLi BohanXie JiongQi JiLi FangyeLiang PanpanHan QiuyingWu MinZhou WenchaoWang ChenhuiZhang WeinaJiang XinZhang KunLi HuiyanZhang XueminLi AilingZhou TaoMan Jianghong