AREB6 EMSA Kit
- Known as:
- AREB6 EMSA Kit
- Catalog number:
- AY1164
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- AREB6 EMSA Kit
Related genes to: AREB6 EMSA Kit
- 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
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- Endothelial-to-mesenchymal transition (EndMT) is a phenotypic switch in which endothelial cells acquire mesenchymal characteristics, involving both functional and morphological changes. While EndMT is essential for cardiac development, its aberrant activation contributes to adult cardiovascular pathologies, including calcific aortic valve disease (CAVD). Dysregulation of ectonucleotidases-membrane-bound enzymes that regulate extracellular ATP and adenosine metabolism-has been implicated in such diseases. Altered extracellular nucleotide signaling influences valvular interstitial cell (VIC) degeneration and may interact with valvular endothelial cells (VECs) undergoing EndMT. The objective of this study was to investigate the role of the purinergic signaling system in regulating EndMT in human aortic VECs. Primary human VECs were cultured in vitro and treated with inhibitors of ectonucleoside triphosphate diphosphohydrolase 1 (CD39), ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1), and 5'-nucleotidase (CD73), alongside adenosine and P2 purinergic receptor agonists. EndMT markers and signaling pathways were assessed via phosphorylation assays and mRNA expression analysis of key transcription factors, including SLUG, SNAIL, ZEB1, and ZEB2. Inhibition of ATP- and AMP-hydrolyzing enzymes (CD39, ENPP1, CD73) enhanced p38 phosphorylation and modulated SLUG expression. Activation of P2 and adenosine A2B receptors altered SNAIL levels, while A2A receptor signaling influenced ZEB1 and ZEB2 expression. These perturbations resulted in pronounced morphological changes consistent with EndMT. In conclusion, dysregulation of the purinergic signaling system induces EndMT in human aortic VECs, highlighting a potential mechanistic link between extracellular nucleotide metabolism and valvular pathology. Targeting purinergic pathways may represent a therapeutic avenue for CAVD and related vascular disorders. - Source: PubMed
Publication date: 2026/04/18
Schmidt VeraWeber AndreasLichtenberg ArturSchrader JürgenMartsch PascalBarth MareikeAkhyari Payam - Gallbladder cancer (GBC) is the most common and aggressive type of tumor occurring in the biliary system. Several studies have indicated the possible functions of circular RNAs (circRNAs) in GBC tumorigenesis. This research aimed to explore the roles of a novel circRNA, circ-ZEB1 (hsa_circ_0093509), in GBC. The expressions of circ-ZEB1, miR-144-3p, and ZEB2 in GBC cells were detected using RT-qPCR or western blot. The subcellular localization of circ-ZEB1 in GBC cells was determined. The function of circ-ZEB1, miR-144-3p, and ZEB2 in GBC cells was assessed by using CCK-8, EdU staining, colony formation, or Transwell assays. The relationship among miR-144-3p and corresponding targets, circ-ZEB1 and ZEB2, was confirmed. Additionally, xenograft experiments were conducted to assess the role of circ-ZEB1 in tumor growth in vivo. circ-ZEB1 was predominantly found in the cytoplasmic region of GBC cells and was upregulated in the GBC cell lines. Suppression of circ-ZEB1 reduced the proliferation and migration of GBC-SD and SGC-996 cells. Knockdown of circ-ZEB1 attenuates tumor growth in vivo. Mechanistically, circ-ZEB1 sponged miR-144-3p, which targeted ZEB2. Additionally, inhibition of miR-144-3p rescues the effects of circ-ZEB1 or ZEB2 knockdown. These results clarified a vital role of the circ-ZEB1/miR-144-3p/ZEB2 axis in GBC advancement, and may serve as a novel therapeutic target for GBC treatment. - Source: PubMed
Huang LuoshunZhang YangYang FanLing YishengZhou Xianfei - Oral cancer (OC) exhibits aggressive growth and metastatic potential. Imipramine, a tricyclic antidepressant, has been recently explored for its anticancer activity. This study investigated imipramine's therapeutic effects and underlying anti-progression mechanisms in OC. - Source: PubMed
Wang Wei-ChunChen Ying-TzuHsu Fei-TingPeng Bing-RuTu Hsi-Feng - 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