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
- Silicosis is caused by occupational exposure to respirable crystalline silica (CS) particles and is characterized by chronic inflammation and progressive pulmonary fibrosis. To date, the underlying mechanisms of silicosis remain poorly understood and effective treatment options are limited. Stimulator of interferon genes (STING) has been identified by us and others as a critical initiator of inflammatory responses and lung damage during silicosis. In this study, we investigate the role of STING pathway in regulating programmed death-ligand 1 (PD-L1) expression and epithelial-mesenchymal transition (EMT) during silicosis, and further explore the underlying mechanisms and profibrotic significance of this axis. Our findings demonstrate that STING signaling regulates PD-L1 expression and promotes EMT progression in the silicosis mouse model. Mechanistically, CS-activated macrophage STING signaling induces PD-L1 expression and drives the EMT process in alveolar epithelial cells by the TGF-β1/Smad2/3 signaling pathway. Furthermore, we demonstrate that epithelial PD-L1 mediates CS-induced EMT and fibrogenic activity in alveolar epithelia. Collectively, these findings extend our mechanistic understanding of how STING promotes silicotic fibrosis and identify potential therapeutic targets for silicosis. - Source: PubMed
Publication date: 2026/08/13
Zhang PengYu MenglingCao YingWei XianZhang XueruDong DinghaoChen Ying - MicroRNAs (miRNAs) are conserved post-transcriptional regulators that play essential roles in cellular development and differentiation. Although miRNAs involved in oligodendrocyte lineage cell (OLLC) differentiation have been extensively studied in rodent models, their functions in human oligodendrocyte (OL) development remain poorly understood. To address this, we used a human embryonic stem cell (hESC) reporter system and an optimized differentiation protocol to generate and isolate well-characterized OLLCs at defined developmental stages. Next-generation sequencing-based miRNA profiling identified stage-specific miRNAs associated with OL lineage specification and maturation. In addition to canonical OL-associated miRNAs, we identified several previously uncharacterized oligodendrocyte progenitor cell (OPC)/oligodendrocyte (OL)-enriched miRNAs, including miR-3943, miR-4286, miR-1296-5p, miR-488-3p, miR-675-5p, and miR-128-3p, as potential novel regulators and molecular markers for human OLLC development. Computational target analysis further identified candidate regulatory genes, including ZNF488, DLX1, CSNK2B, and KCNJ1, and predicted their association with AKT, SMAD2/3, estrogen-receptor, and insulin-signaling pathways. Together, these findings provide a comprehensive stage-specific miRNA resource for human OL lineage development and provide insight into potential miRNA-mediated regulatory networks governing human OL development. - Source: PubMed
Publication date: 2026/07/27
Barzegar MansourehDhukhwa AsmitaPatel Vaidehi NileshVelasquez Fernanda CDas SamarjitPatil Arun HHalushka Marc KChamling Xitiz - Osteoarthritis (OA) is a debilitating degenerative joint disease marked by the progressive breakdown of cartilage, synovium, and subchondral bone. This comprehensive narrative review synthesizes findings from recent foundational and preclinical studies to elucidate the complex, concentration and context-dependent functional dichotomy of the transforming growth factor-beta (TGF-β) signaling pathway in OA pathophysiology. At physiological levels, TGF-β signaling via the canonical SMAD2/3 pathway promotes chondrocyte anabolism, whereas aberrant overactivation, often through the SMAD1/5/8 axis, drives pathological processes including chondrocyte hypertrophy, synovial fibrosis, and aberrant bone remodeling. However, these signaling outputs are not fixed; they are highly dependent on the specific tissue compartment, disease stage, receptor profile, and the local inflammatory microenvironment, which collectively dictate the ultimate functional outcome. While conventional systemic interventions lack the precision to differentially modulate these opposing functions, engineered biomaterials have emerged as versatile platforms for achieving spatiotemporally precise regulation. We detail key strategies employing hydrogels, nanocarriers, and functionalized scaffolds that enable targeted therapeutic outcomes through controlled delivery, receptor blockade, or downstream pathway intervention. Although these biomaterial-based strategies remain predominantly at the experimental and preclinical stage, they represent a conceptually advanced approach to addressing this therapeutic dilemma. Future directions must focus on overcoming major translational barriers-including joint retention, targeting specificity, long-term biosafety, manufacturing reproducibility, and precise patient and disease-stage stratification-to advance these strategies toward clinical utility. - Source: PubMed
Publication date: 2026/08/06
Peng PengXia LuShang Xiaobin - Chronic stress commonly precipitates telogen effluvium (TE), but sustained stress can further induce follicular miniaturization and fibrosis. Thus, stress-induced alopecia may be considered a pathological continuum that progresses from TE to fibrotic follicular degeneration. Stress-induced alopecia involves multiple pathological mechanisms including follicular fibrosis, miniaturization and hair thinning. Currently, there is a lack of systematic therapeutic approaches targeting its multi-target pathological processes. This study proposes a novel combination strategy (EBP: EGCG, Biotin and Pal-GHK) designed to synergistically modulate the TGF-β/Smad and BMP signaling pathways to target key pathological processes in stress-induced alopecia. Through molecular docking, cell co-culture experiments, animal models and microbial interaction analysis, the EBP combination was systematically evaluated for its effects in inhibiting follicular fibrosis, promoting follicular regeneration and enhancing keratin synthesis. The results demonstrated that EBP effectively inhibited TGF-β/Smad pathway and activated BMP pathway. In the stress-induced fibrotic alopecia mouse model, compared to the Model group, the High EBP group significantly upregulated BMP2 by 2.77-fold, while downregulating TGF-β1 and P-Smad2 expression levels to 35.7% and 65.9%, respectively. These molecular changes were accompanied by substantial improvements in hair follicle morphology, hair shaft quality and hair regrowth. Furthermore, microbial biotransformation of EBP components may contribute to prolonged biological activity and sustained therapeutic efficacy. This study provides novel theoretical and experimental evidence for multi-target combined therapy in stress-induced alopecia. - Source: PubMed
Publication date: 2026/08/10
Zheng XiaodanWang NaMa HeweiXu ZhenyuWu WeilingLiu WenyuanFu MeixiHan Lingfei - Lung cancer remains the most common cause of cancer-related mortality worldwide. The transforming growth factor-beta 1 (TGF-β1) pathway promotes epithelial-mesenchymal transition (EMT), invasion, and metastasis in advanced disease via mothers against decapentaplegic homolog 2 (Smad2) and Smad3. This study investigated how post-translational modifications regulate TGF-β1-Smad signaling. - Source: PubMed
Publication date: 2026/08/10
Li YulongZhou YuZhao PengShi MinWang ZhiyanZhang ZhijianQu Geping