Esrp2 Antibody - N-terminal region (ARP37937_P050)
- Known as:
- Esrp2 Antibody - N-terminal region (ARP37937_P050)
- Catalog number:
- arp37937_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- Esrp2 Antibody - N-terminal region (ARP37937_P050)
Related genes to: Esrp2 Antibody - N-terminal region (ARP37937_P050)
- Gene:
- ESRP2 NIH gene
- Name:
- epithelial splicing regulatory protein 2
- Previous symbol:
- RBM35B
- Synonyms:
- FLJ21918
- Chromosome:
- 16q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-09-22
- Date modifiied:
- 2019-02-20
Related products to: Esrp2 Antibody - N-terminal region (ARP37937_P050)
Related articles to: Esrp2 Antibody - N-terminal region (ARP37937_P050)
- Hepatocellular carcinoma (HCC) is one of the most metastatic and aggressive malignancies. Circular RNAs (circRNAs) are associated with the pathogenesis and prognosis of HCC. This study aimed to explore the role of circ_0020236 in HCC progression. Expression levels of circ_0020236, miR-1825, and IKBKB were assessed in HCC clinical samples and cell lines using quantitative real-time PCR. Bioinformatics predictions combined with dual-luciferase reporter, RNA immunoprecipitation, and RNA pull-down assays validated molecular interactions. Functional assays, including CCK-8, colony formation, and Transwell migration, were employed to evaluate cell proliferation and migration. The results indicated that circ_0020236 and IKBKB were significantly downregulated, whereas miR-1825 was upregulated in HCC. Ectopic expression of circ_0020236 suppressed HCC cell proliferation, migration, and tumor growth in vivo. Mechanistically, circ_0020236 functioned as a molecular sponge for miR-1825, which directly targeted IKBKB. Rescue experiments showed that miR-1825 overexpression reversed the tumor-suppressive effects of circ_0020236, while IKBKB knockdown abrogated the inhibitory phenotype induced by miR-1825 silencing. Furthermore, the RNA-binding protein ESRP2 was identified as a positive regulator of circ_0020236 biogenesis. In conclusion, our findings reveal that the ESRP2/circ_0020236/miR-1825/IKBKB axis plays a critical role in inhibiting HCC progression, positioning circ_0020236 as a promising therapeutic target for HCC intervention. - Source: PubMed
Publication date: 2026/05/13
Liu JingSun BingCao PengZhou Sufang - 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 - Epithelial splicing regulatory protein 2 (ESRP2) is a splicing regulator specific to epithelial cell types. Multiple studies have found that its expression is abnormal in various tumors, influencing their occurrence, development, or prognosis. Our previous research indicated that down-regulating ESRP2 can suppress the proliferation of breast cancer (BC) cells, specifically the MCF-7 line. To delve deeper into the role of ESRP2 in BC cells, we investigated its impact on the migration of BC cells in vitro and the underlying molecular mechanisms. The outcomes of the in vitro scratch assay and Transwell assay initially confirmed that ESRP2 hinders the migration of both MCF-7 and MDA-MB-231 cells, and that reducing ESRP2 expression enhances their migratory capacity. We demonstrated that the down-regulation of ESRP2 can boost the migration ability of MCF-7 cells, and increase the mRNA expression of epithelial-mesenchymal transition (EMT) transcription factor ZEB2 and related markers N-cadherin and Vimentin. This suggests that ESRP2 plays a potential regulatory role in inhibiting EMT transcription program. Additionally, results from RNA sequencing and agarose electrophoresis gel experiments predict that down-regulating ESRP2 may promote exon skipping of the ENAH gene by modulating the alternative splicing of genes associated with cell migration, driving the shift of MCF-7 cells from an epithelial to a mesenchymal phenotype. Our research reveals a novel mechanism by which ESRP2 affects BC metastasis through post-transcriptional regulation. ESRP2 may present as a promising biomarker in combating BC cell migration by targeting EMT. - Source: PubMed
Publication date: 2026/02/10
Chen YutingFeng HuancunZhao ChengkuanHuang LintingLiao ZirouChen WangZou JianZhang Shuyao - Adipose tissue exhibits remarkable plasticity, defined as its capability of adapting to various environments and energy demands by undergoing shifts in phenotypic, metabolic characteristics, and structure. However, obesity often results in diminished adipose tissue plasticity. Long non-coding RNA (lncRNA) is a class of RNA defined as being more than 200 nucleotides long and lacking protein-coding capability. With advancements in ribosome profiling, mass spectrometry, and other research technologies, an increasing number of studies have confirmed that short open reading frames (less than 300 nucleotides) within lncRNAs have the capacity to encode functional micropeptides. In our study, we initially identified a biologically active micropeptide, lncRNA Esrp2-as-ORF1(LEAO), encoded by lncRNA Esrp2-as in mice. In diet-induced obesity (DIO)mice, this micropeptide demonstrates the ability to induce fat browning, enhance adipose tissue plasticity, and subsequently improve metabolic homeostasis. Additionally, we observed that the micropeptide LEAO exerts its effects on adipocytes by stimulating IL6 secretion in adipose tissue macrophages. In summary, LEAO may have therapeutic potential for obesity-related metabolic diseases. - Source: PubMed
Publication date: 2026/01/27
Liu SiqiSong BiguiHu LongyunZhao ZeweiLi JinLi XiaoxiaoQian BingxiuCai YiLin JiejingWu QianSun XianYang Zhonghan - The pituitary gland produces several hormones that regulate growth, metabolism, stress response, reproduction and homeostasis. Congenital hypopituitarism is a deficiency in one or more pituitary hormones and encompasses a spectrum of clinical conditions. The pituitary has a complex embryonic origin, with the oral ectoderm contributing the anterior lobe, and the neural ectoderm generating the posterior lobe. Pituitary abnormalities and growth deficiencies are associated with cleft palate; however, the developmental genetic connection between pituitary and orofacial cleft malformations remains to be determined. The epithelial RNA splicing regulators Esrp1 and Esrp2 (Esrp1/2) are required for orofacial development in zebrafish, mice and humans, and loss of function of these genes results in a cleft palate. Here, we present a detailed developmental analysis of the genetic requirement for Esrp1/2 in pituitary morphogenesis in mouse and zebrafish. Further, we describe an individual with cleft palate and hypopituitarism who harbors a nucleotide variant in the RNA-binding domain of ESRP2. The discovery of this key function for Esrp1/2 in pituitary formation has significant fundamental and clinical implications for understanding congenital hypopituitarism and craniofacial anomalies. - Source: PubMed
Publication date: 2025/10/30
Carroll Shannon HSchafer SogandRichman Ariella SWang PengAhsan Mian UmairTsay LisaWang KaiLiao Eric C