AREB6 EMSA Probe Set
- Known as:
- AREB6 EMSA Probe Set
- Catalog number:
- AY1164P
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- AREB6 EMSA Probe Set
Related genes to: AREB6 EMSA Probe Set
- Gene:
- ZEB1 NIH gene
- Name:
- zinc finger E-box binding homeobox 1
- Previous symbol:
- TCF8, PPCD3
- Synonyms:
- BZP, ZEB, AREB6, NIL-2-A, Zfhep, Zfhx1a, FECD6
- Chromosome:
- 10p11.22
- Locus Type:
- gene with protein product
- Date approved:
- 1991-12-17
- Date modifiied:
- 2014-11-19
Related products to: AREB6 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: AREB6 EMSA Probe Set
- Glioma is the most aggressive tumor of the central nervous system and is associated with poor prognosis, especially in patients with high-grade gliomas. In this study, we investigated the biological role of inhibitor of kappa B kinase interacting protein (IKBIP) in promoting the progression of glioma. Analysis of the TCGA and GTEx databases revealed that IKBIP is upregulated in both lower-grade gliomas (LGG) and glioblastomas (GBM) compared with normal brain tissues. Kaplan-Meier survival analysis demonstrated that IKBIP upregulation is associated with shorter overall survival (OS) and disease-specific survival (DSS) in patients with LGG. Pan-cancer analysis indicated that IKBIP is aberrantly expressed in various malignant tumors, including gliomas. IKBIP knockdown inhibited the proliferation of glioma cells both and . Additionally, IKBIP knockdown in U251 and U87 glioma cell lines significantly suppressed their invasive capacity. Furthermore, IKBIP knockdown resulted in decreased expression of proteins associated with Wnt/β-catenin/epithelial-mesenchymal transition (EMT) pathway, including β-catenin, ZEB1, ZEB2, N-cadherin, whereas the expression of E-cadherin was increased. Conversely, IKBIP overexpression reduced the level of phosphorylated β-catenin (p-β-catenin) while increasing the expression of total β-catenin in glioma cells. Furthermore, we identified that transcription factor SP1 (Specificity Protein 1), which is also upregulated in glioma tissues and cell lines and is associated with the malignant phenotype of glioma, can bind to the promoter region of IKBIP. Upregulation of SPI in glioma cells significantly increased the expression level of IKBIP, while inhibiting the phosphorylation of β-catenin. These findings collectively suggest that upregulation of IKBIP promotes the proliferation and invasive behaviors of glioma cells by activating the Wnt/β-catenin/EMT pathway. Overall, our findings suggest that SP1-IKBIP axis facilitates the proliferation and invasion of glioma through Wnt/β-catenin-associated EMT, and SP1-IKBIP axis may represent a promising target for the clinical diagnosis and treatment of glioma. - Source: PubMed
Publication date: 2026/03/25
Liu NanZhao MingyueXu LeiCui YetingTian YuLi JuanHu XiaoyuZhang TongcunZhen HainingTu Yanyang - Multiple sclerosis (MS) is a multifactorial autoimmune condition, and existing medications offer limited efficacy, especially regarding the control of disease progression. Our previous research has suggested a significant role for ferroptosis in the mechanism of MS, making it a promising therapeutic target. - Source: PubMed
Publication date: 2026/04/16
Wu TaoCao YuzeWang LihuaWang ZhaoxiaHao HongjunZhang Huixue - Epithelial-mesenchymal transition drives tumor metastasis and therapeutic resistance, yet few treatments have been developed that target this process. Here, we show that ELMO2 represents a specific vulnerability in mesenchymal-like cells. ELMO2 suppression induces excessive autophagy and cell death via FAK activity inhibition. We identify ELMO3 as a functional paralog that compensates for ELMO2 loss, establishing a synthetic lethal interaction. The epithelial-mesenchymal transition core regulator ZEB1 represses ELMO3 transcription in mesenchymal-like cells, rendering them sensitive to ELMO2 blockade. ELMO3 is significantly downregulated in epithelial-mesenchymal transition-associated EGFR inhibitor-resistant cells. Furthermore, the survival of these resistant, mesenchymal-like cells depends on ELMO2/FAK signaling. Through structure-based screening, we identify C52, a small-molecule ELMO2 inhibitor that effectively kills ELMO3-low lung cancer cells and EGFR inhibitor-resistant cells. Our study uncovers an ELMO2-ELMO3 synthetic lethal interaction and establishes ELMO2 as a potential therapeutic target for mesenchymal-like cancer and drug-resistant non-small cell lung cancer. - Source: PubMed
Publication date: 2026/04/17
Li MinXue YingChang YuhanXu FanWu FeizhenTian XinjianHu JieSong YijunYu XufenZhou FeiZhou CaicunCao XinWang MeiHuang Qihong - Epithelial-to-mesenchymal transition (EMT)-driven phenotypic plasticity promotes bladder cancer (BC) progression and therapy resistance. While EMT has been primarily associated with transcriptional reprogramming, the contribution of post-transcriptional mechanisms, particularly alternative splicing regulation, remains insufficiently explored. This study aimed to investigate the clinical significance and mechanistic role of epithelial splicing regulatory protein 2 (ESRP2) in BC. - Source: PubMed
Publication date: 2026/03/30
Bajdak-Rusinek KarolinaJankowska KarolinaSundararajan VigneshSieroń ŁukaszDiak NataliaWójtowicz WeronikaStępień Karolina LFus-Kujawa AgnieszkaGutmajster EwaWierzbinka MateuszZorychta Kinga - This study aims to utilize multiomics and bioinformatics techniques to investigate the expression of the connection enzyme inhibitor Ras1 1 (CNKSR1) in ovarian cancer (OC) and its mechanism of action in the processes of tumor proliferation, invasion, and metastasis. Transcriptome sequencing was performed on paired cancerous and normal ovarian tissues from three OC patients. Differentially expressed genes (DEGs) mRNAs were analyzed using "limma", and key DEGs were identified through LASSO and random forest (RF) methods. expression in OC tissues was assessed via quantitative reverse transcription polymerase chain reaction (qRT-PCR), Western blot, and immunohistochemistry. Gene Ontology (GO) enrichment analysis was conducted utilizing the Database for Annotation, Visualization, and Integrated Discovery (DAVID), and CancerSEA was employed to assess the functional status of in OC. Also, the proliferation of cells, their invasion, and migration were evaluated. ChEA3 and hTFtarget were used to identify potential transcription factors targeting . The predicted factors were validated by Western blot analysis in OC cells overexpressing or in OC cells with the knockdown. Compared to normal tissues, 78 genes were downregulated, and 101 were upregulated in OC. LASSO and RF analyses identified as a vital gene positively correlated with the progression of OC, which was then experimentally validated. upregulation promoted the OC cells' proliferation, their invasion, and migration, while its silencing inhibited these processes. Analysis of the ChEA3 and hTFtarget databases, as well as Western blot analysis, suggested that may drive epithelial-mesenchymal transition (EMT) by upregulating snail and ZEB1 expression. serves a significant role in promoting the growth and progression of OC. It enhances OC cells' metastatic and invasive abilities by regulating the EMT mediated by the transcription factors Snail and ZEB1. - Source: PubMed
Publication date: 2026/04/11
Zhu WeiliHuang YiminHuang JiayueWang JianguoShen Sijia