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
- Cardiac fibrosis is a central driver of adverse remodeling and heart failure (HF), yet effective antifibrotic therapies remain limited. SerpinA3, a member of the serine protease inhibitor family, has been implicated in cardiovascular disease, but its functional role and underlying mechanisms in cardiac remodeling are poorly defined. - Source: PubMed
Publication date: 2026/08/30
Wang HuiCui JieyuHuang ChunluGuo WanyiLiu TongZhu YiShao ShuaiChen KangyinHe JinlongBao Qiankun - Lymphedema is a chronic disease characterized by impaired lymph drainage and accumulation of protein-rich interstitial fluid, which progresses to develop irreversible fibrosis. Despite its substantial clinical burden, effective pharmacological therapies that improve lymphatic function and prevent disease progression remain lacking. Given the prominent inflammatory and fibrotic responses associated with lymphedema, we investigated the therapeutic potential of IVA337 (lanifibranor), a pan-peroxisome proliferator-activated receptor (PPAR) agonist that activates PPARα, PPARβ/δ, and PPARγ, key regulators of lipid metabolism, inflammation, and fibrosis. Here, we evaluated the therapeutic efficacy of IVA337 during the early stage of surgery-induced secondary lymphedema in mice and investigated the underlying mechanisms. IVA337 administration alleviates lymphedema progression, improves lymphatic drainage, reduces dermal thickness, and resolves lymphatic vessel dilation. Mechanistically, IVA337 suppresses TGFβ/SMAD2/3 signaling pathway, reduces immune cells infiltration, and improves lymphatic vessels integrity. In human dermal lymphatic endothelial cells (HDLECs), IVA337 attenuates TGFβ induced SMAD2/3 phosphorylation and preserves the expression of cell junction Claudin5, reduces VE-Cadherin-stained cell-cell gaps. Collectively, our findings demonstrate that IVA337 protects against early-stage lymphedema by suppressing TGFβ/SMAD2/3 signaling and limiting inflammatory and fibrotic and lymphatic endothelial dysfunction. These findings identify pan-PPAR activation as a promising pharmacological strategy to preserve lymphatic function during the early phase of lymphedema and potentially prevent progressive tissue fibrosis. - Source: PubMed
Publication date: 2026/08/29
Pang JingjingDo Long Nguyen HoangDelgado EstebanZhao JiananFlynn LiamLiu HongxiaAutieri MichaelYang XiaofengLiu Xiaolei - Epithelial-mesenchymal transition (EMT) is crucial for initiation of cancer metastasis. EMT-induced epithelial cancer cells gain stemness characteristics, which enhance cancer malignancy and chemoresistance. Therefore, it is important to clarify the function of EMT-related genes for development of therapeutics for cancer metastasis. Here, we showed that Signal-transducing adaptor protein-2 (STAP-2) inhibits EMT in cancer cells through repressing SMAD-mediated ZEB1 expression, which is a master transcription factor of EMT. STAP-2 inhibits the interaction between SMAD3 and SMAD4, resulting in the downregulation of SMAD2/3/4 complex formation and TGF-β signal-induced gene expression. STAP-2 expression was repressed by SMAD2/3-mediated TGF-β signals and activated by OVOL1, which is one of the EMT repressor transcription factors. Our study showed that STAP-2 is a novel EMT repressor gene which represses ZEB1 expression and motility of cancer cells. - Source: PubMed
Okuyama FumiyaKitai YuichiLi ZhengchengIshii MikitoMuromoto RyutaMatsuda Tadashi - Idiopathic pulmonary fibrosis (IPF) is characterized by aberrant fibroblast proliferation and excessive expression and deposition of extracellular matrix (ECM) by myofibroblasts, ultimately resulting in progressive and irreversible disorder or even loss of the pulmonary function. IPF is incurable with limited therapeutic options and low survival rate, thus the discovery of the therapeutic potential agents for IPF is in urgent need. Here, we identified isopropyl 9-ethyl-1-(naphthalen-1-yl)-9H-pyrido[3,4-b] indole-3-carboxylate (Z86) as a promising bioactive agent against Bleomycin (BLM) induced pulmonary fibrotic mice with the lung abnormalities including histological alteration, accumulation of ECM, as well as markers of EMT (epithelial-mesenchymal transition) were all relieved upon Z86 treatment in C57BL/6 mice. Consistent to the activity in vivo, Z86 decreased TGF-β induced cell migration, fibrotic marker expression, and myofibroblast activation in A549 and HFL1 cells. In further mechanism of action study of Z86 against IPF, we found TGF-β (transforming growth factor β) /Smad2/3 signaling pathway was substantially attenuated in TGF-β treated A549 and HFL1 cells, with remarkably decreased protein level of Smad2/3. Further, we identified Z86 as a novel USP15 inhibitor. Correspondingly, Z86 interacted with USP15, promoted the ubiquitination and degradation of Smad2/3 and disrupted TGF-β/Smad2/3 signaling pathway. Taken together, our findings demonstrated that Z86 suppressed TGF-β induced pulmonary fibrosis in A549 and HFL cells and BLM induced pulmonary fibrotic mice through inhibiting TGF-β/Smad2/3 signaling, and provided the possibility of USP15 inhibitors as the potential drug candidates for idiopathic pulmonary fibrosis. - Source: PubMed
Publication date: 2026/08/28
Wang YuyangZhang ShaohuaGeng RongWang RuiyingHuang YingXu GangKong LingmeiLi Yan - Renal fibrosis is a common pathological outcome of chronic kidney disease and is characterized by persistent profibrotic signaling and impaired cellular homeostasis. Genkwanin (GAK), a natural flavonoid compound, has shown anti-inflammatory and antioxidant activities in several disease models. However, its role in renal fibrosis remains unclear. - Source: PubMed
Publication date: 2026/08/13
Wang ShenHe YuGan XinKang HaoZhou ZhuHe ZongHai