Smad2 (Phospho_Thr220) Antibody
- Known as:
- Smad2 (Phospho_Thr220) Antibody
- Catalog number:
- E011323-2
- Product Quantity:
- 100ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- Smad2 (Phospho_Thr220) Antibody
Related genes to: Smad2 (Phospho_Thr220) Antibody
- Gene:
- SMAD2 NIH gene
- Name:
- SMAD family member 2
- Previous symbol:
- MADH2
- Synonyms:
- MADR2, JV18-1
- Chromosome:
- 18q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-11-15
- Date modifiied:
- 2016-10-05
Related products to: Smad2 (Phospho_Thr220) Antibody
Related articles to: Smad2 (Phospho_Thr220) Antibody
- Cartilage fibrosis contributes to extracellular matrix remodelling and structural deterioration during osteoarthritis (OA) progression; however, the molecular regulators involved in this process remain incompletely understood. Stanniocalcin-1 (STC1) has been implicated in tissue remodelling and fibrosis-associated signalling, but its role in chondrocyte fibrotic phenotype transition remains unclear. In this study, primary mouse chondrocytes stimulated with interleukin-1β (IL-1β), a destabilization of the medial meniscus (DMM) mouse model, and human OA cartilage samples were used to investigate the involvement of STC1 in OA-associated fibrotic remodelling. Quantitative proteomic profiling identified STC1 as a differentially regulated candidate associated with inflammatory and fibrotic responses. STC1 expression was elevated under OA-related conditions and was accompanied by increased SMAD2/3 phosphorylation. In SW1353 chondrosarcoma-derived chondrocytic cells, STC1 overexpression enhanced fibrosis-associated phenotypic changes, including increased COL1A1, ADAMTS5, and MMP-3 expression, reduced COL2A1 expression, and increased SMAD2/3 phosphorylation. Pharmacological modulation experiments further supported an association between STC1 and TGF-β/SMAD2/3 signalling activity. Artemotil attenuated fibrotic and catabolic responses in IL-1β-stimulated chondrocytes, reduced cartilage degeneration in DMM-induced OA, and was associated with reduced STC1 expression and reduced SMAD2/3 phosphorylation. Restoration of STC1 expression partially attenuated the effects of Artemotil on fibrosis-related markers and signalling alterations. These findings support a functional association between STC1, TGF-β-responsive SMAD2/3 signalling, and fibrosis-associated chondrocyte remodelling in OA and identify this signalling relationship as responsive to Artemotil intervention. - Source: PubMed
Zhu GuangYang YangMa YeWu GangTian KuanminHe XiaoxinWang RuiMa PenggangTang ZhiqunJin Qunhua - Hepatocellular carcinoma (HCC) progression and metastasis are closely associated with the acquisition and maintenance of a mesenchymal phenotype. The transforming growth factor (TGF)-β/SMAD signaling pathway stabilizes the mesenchymal state of HCC, whereas the inflammatory cytokine interleukin-1β (IL-1β) is abundantly expressed in the HCC tumor microenvironment and activates p38 mitogen-activated protein kinase (MAPK), a key mediator of cell migration and invasion. However, the role of inflammatory cytokines in modulating TGF-β-mediated mesenchymal phenotypes remains unclear. Therefore, this study aimed to determine the function of IL-1β in the regulation of mesenchymal phenotypes in SK-Hep1 cells and elucidate the roles of the TGF-β/SMAD and p38 MAPK signaling pathways. - Source: PubMed
Publication date: 2026/09/16
Fatima SaherRegmi BhupendraHwang SoonjaeKim Moon YoungBaik Soon KooJung Pil YoungEom Young Woo - [This retracts the article DOI: 10.3389/fcell.2020.573781.]. - Source: PubMed
Publication date: 2026/09/01
- To determine the role of Zinc finger E-box binding homeobox factor 1 (ZEB1) in pulmonary sarcomatoid carcinoma (PSC), we determined whether its expression in 40 PSC and 100 papillary lung carcinoma (Pap-LC) samples correlates. PSC patients with high ZEB1 had a significantly poorer prognosis when compared with Pap-LC; this was also the case for epithelial-to-mesenchymal transition (EMT) factor Slug, but not Snail or Twist1. A combined ZEB1-high and Slug-high scores appeared to be associated with the worst prognosis in PSC, suggesting that this metric may have great utility in predicting disease progression. ZEB1 was transcriptionally upregulated by the TGF-β1/Smad2 axis and ZEB1/Slug feedback loop, leading to repression of E-cadherin and induction of EMT/cancer stem cell (CSC) properties. Reduced ZEB1 expression due to ubiquitin-proteasomal degradation was associated with giant/senescent cell phenotypes. Consistent with this, ZEB1 expression was lowest in PSC samples with a high proportion of giant/senescent cell types, where prognosis was favorable. Increased expression of p21, p16, and ubiquitin was concomitant with reduced ZEB1. Together, our findings reveal novel mechanistic insight into the establishment and maintenance of PSC phenotypes through ZEB1-dependent induction of EMT/CSC properties and suppression of senescence. - Source: PubMed
Ono MototsuguEndo ShinyaTochimoto MasatakaYokoi AkoOguri YasukoHashimura MikiHara HiroikuSatoh YukitoshiSaegusa Makoto - Pancreatic ductal adenocarcinoma (PDAC) is characterized by early metastatic dissemination and poor clinical outcomes. Although SMAD4 is frequently altered in PDAC, the majority of tumors retain wild-type SMAD4, which paradoxically acquires pro-metastatic functions during disease progression. Uncovering how SMAD4 transcriptional output is reprogrammed to support metastasis in advanced PDAC could reveal strategies to prevent and treat metastasis. Here, we identified protein arginine methyltransferase 1 (PRMT1) as a critical modifier that mediates a metastasis-promoting transcriptional state of SMAD4. PRMT1 catalyzed asymmetric dimethylation of SMAD4 at arginine 272 (R272), a modification that did not alter SMAD4 expression but stabilized nuclear SMAD2/3-SMAD4 complexes and redirected SMAD4 chromatin engagement toward epithelial-mesenchymal transition (EMT) gene programs. Mechanistically, R272-methylated SMAD4 promoted the recruitment of a BRG1-CTCF transcriptional complex, enabling chromatin-dependent activation of pro-metastatic transcriptional outputs. Importantly, pharmacological inhibition of PRMT1, particularly in combination with BRG1 degradation, dismantled methylation-dependent SMAD4 transcriptional complexes, suppressed EMT programs, and markedly reduced liver metastasis in preclinical PDAC models. Together, these findings uncover a post-translational mechanism that governs SMAD4 transcriptional specificity and identify PRMT1-dependent methylation as a therapeutic vulnerability in SMAD4-wild-type pancreatic cancer. - Source: PubMed
Publication date: 2026/09/15
Liu YizhouLiang XueyiWei RuozhengPeng YuQin GengduLiu JiayingZhao YuhanCai HongkunChen TaoyuGou ShanmiaoYin TaoWang BoWu HeshuiZhou Yingke