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
- Coronary artery disease (CAD) may progress to ischemic cardiomyopathy (ICM) and heart failure through maladaptive cardiomyocyte remodeling and myocardial fibrosis. This study aimed to identify key molecular mediators linking inflammatory and fibrotic signaling during this pathological transition. - Source: PubMed
Publication date: 2026/09/11
Chen KexinHe XingyuNing XiangmingWang YaoLi NaHu TengMa ZeyuanYang FengruiZhang YinleiMa JunShi Zheng - Pathological scarring is driven by persistent crosstalk between profibrotic cytokine signaling and extracellular matrix remodeling. Transforming growth factor-β1 (TGF-β1)/Smad2/3 signaling broadly activates fibroblasts, whereas bone morphogenetic protein 2 (BMP2)/Smad1/5/9 signaling reinforces matrix-producing fibroblast states. Concurrent modulation of these pathways may therefore provide a more comprehensive therapeutic strategy. - Source: PubMed
Publication date: 2026/09/11
Wang YangmeihuiXian JunRen ShuyaLin XiaomianChen QiuyuLiang XiaofengDeng ChengchengYang Bin - To investigate the expression of SYTL5 in differentiated thyroid carcinoma (DTC) and elucidate its clinical significance and underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/09/03
Zhu XiaohuiPan XiaJiang DongmeiCui HengfengWu HaiyanWang YuyingLi Xia - Intrauterine adhesion (IUA) is characterized by endometrial fibrosis, impaired vascularization, and loss of endometrial receptivity, resulting in infertility and adverse reproductive outcomes. Current clinical treatments remain limited because of inadequate tissue regeneration and high rates of adhesion recurrence. While hydrogel-based therapeutics show promise, their clinical translation is frequently hindered by potential cytotoxicity from chemical crosslinkers and the absence of multifaceted bio-inductive niches. Herein, we present a highly translatable, cell-free strategy utilizing a physically crosslinked, injectable thermosensitive hydrogel composed of Poloxamer 407 (P407) and natural Hyaluronic Acid (HA) to deliver platelet-derived factors (PDFs) for comprehensive endometrial repair. By eschewing chemical modifications, this pristine formulation ensures superior biosafety, rapid in situ gelation tailored to complex uterine morphologies, and optimized sustained-release kinetics. In a rat model of IUA, PDFs@Gel treatment significantly improved endometrial morphology, including increased endometrial thickness and gland number, while reducing fibrosis compared with untreated IUA animals. Immunofluorescence and western blot analyses further demonstrated enhanced expression of CK18, Vimentin, VEGF-A, and VEGF-R2 after treatment, indicating improved epithelial and stromal regeneration together with enhanced angiogenesis-associated activity. Meanwhile, reduced TGF-β expression and a decreased pSmad2/3-to-Smad2/3 ratio supported suppression of TGF-β/Smad-mediated fibrotic signaling. Reproductive evaluation further showed improved embryo implantation and live birth outcomes following PDFs@Gel administration. Collectively, these findings suggest that PDFs@Gel represents a promising biomaterial strategy for endometrial repair and functional recovery in IUA. STATEMENT OF SIGNIFICANCE: Rather than serving solely as a drug carrier or anti-adhesion barrier, the proposed hydrogel functions as a multifunctional regenerative platform that combines structural protection with sustained delivery of platelet-derived regenerative cues. The physically crosslinked hyaluronic acid/Poloxamer 407 network offers a simple and potentially translatable design without chemical modification or additional crosslinkers. By simultaneously addressing fibrosis, tissue regeneration, and fertility restoration, this study demonstrates a practical biomaterial design strategy for intrauterine applications and provides a translational platform for regenerative therapies requiring simultaneous anti-adhesion and tissue-repair functions. - Source: PubMed
Publication date: 2026/09/16
Jin TongTian LixingShao WentaoLong YuanyuanLi JunxiaLiu JingxiaZhou XingXu Xiang - 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