Smad2 (Phospho-Ser465) Antibody
- Known as:
- Smad2 (Phospho-Ser465) Antibody
- Catalog number:
- 11838
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- Smad2 (Phospho-Ser465) Antibody
Related genes to: Smad2 (Phospho-Ser465) 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-Ser465) Antibody
Related articles to: Smad2 (Phospho-Ser465) Antibody
- Cardiac fibrosis is a pivotal pathological process driving heart failure following ischemia-reperfusion (I/R) injury. STC1 (stanniocalcin-1), a conserved glycoprotein with mitochondrial regulatory functions, remains unexplored in myocardial fibrosis. This study investigates the mechanistic role of cardiomyocyte-derived STC1 in cardiac fibrosis. - Source: PubMed
Publication date: 2026/07/03
Wang XiaoQin FenLi YanTang XiaojieAisa ZulibiyaZhang Baojian - The effects of TGF-βs (transforming growth factor-βs) in failing hearts involve cell-specific actions mediated through receptor-regulated Smads or Smad-independent pathways. The inhibitory Smad, Smad7, is a negative feedback regulator that restrains excessive TGF-β/receptor-regulated Smad signaling, while also exerting TGF-β-independent effects. We hypothesized that cardiomyocyte Smad7 upregulation contributes to the pathogenesis of pressure overload-induced heart failure and investigated the mechanisms underlying its actions. - Source: PubMed
Publication date: 2026/07/03
Humeres ClaudioTuleta IzabelaQin DongzeShinde Arti VDeepak AadyaHanna AnisFrangogiannis Nikolaos G - Postoperative peritoneal adhesion (PPA) is a common complication following abdominal surgery and effective preventive strategies remain limited. The present study aimed to investigate the protective effect of aspirin against PPA in rats and to elucidate the underlying mechanism involving the transforming growth factor‑β1 (TGF‑β1)/Smad signaling pathway. A total of 32 male Sprague‑Dawley rats were randomly divided into the four following groups: Sham‑operated group, model group, low‑dose aspirin group (10 mg/kg) and high‑dose aspirin group (30 mg/kg). A PPA model was established by cecal wall abrasion. The aspirin‑treated groups received daily intragastric administration for 8 consecutive days post‑surgery. All animals were euthanized on day 8. Adhesion severity was assessed using the Nair scoring system; histopathological changes were examined by Masson's trichrome staining; the expression levels of proteins related to the TGF‑β1/Smad pathway and to markers of fibrosis were detected by western blot, immunohistochemical (IHC) and reverse transcription‑quantitative PCR (RT‑qPCR) analyses. In addition, rat primary peritoneal mesothelial cells (RPMCs) were treated with different concentrations of aspirin to evaluate the expression levels of the relevant proteins. The results indicated that compared with the model group, aspirin administration significantly reduced PPA scores. Histological examination revealed that aspirin treatment alleviated collagen deposition in adhesion tissues. The results derived from western blotting, IHC and RT‑qPCR analyses demonstrated that aspirin downregulated the expression levels of TGF‑β1, phosphorylated (p)‑Smad2/3, alpha smooth muscle actin (α‑SMA) and collagen type I, alpha 1 (COL1A1), and inhibited the phosphorylation of Smad2/3. Moreover, treatment of RPMCs with different concentrations of aspirin led to a dose‑dependent decrease in the protein expression levels of TGF‑β1, COL1A1, α‑SMA, p‑Smad2 and p‑Smad3, while simultaneously upregulating the expression levels of the endogenous inhibitory factor Smad6 in this pathway. In conclusion, the data demonstrated that aspirin effectively prevented the formation of PPA in rats by suppressing peritoneal fibrosis, an effect likely mediated via inhibition of the TGF‑β1/Smad signaling pathway. These findings suggest that aspirin is a promising candidate for the clinical prevention of PPA. - Source: PubMed
Publication date: 2026/07/03
Yan SiqiRen YuanLiu BingyanXiong PaiSun Yimin - Recent findings indicate attenuated myostatin (MSTN) signalling in idiopathic inflammatory myopathies (IIM) and an inverse association between circulating MSTN and disease activity. The temporal and mechanistic relationship of these alterations to disease pathogenesis remains unclear. We therefore investigated systemic and skeletal muscle MSTN regulation in newly diagnosed patients at disease onset, after six months of therapy, and in chronic IIM. - Source: PubMed
Publication date: 2026/07/02
Vernerová LuciaLážnovská LucieBaloun JiříBalounová VeronikaVokurková MartinaKlein MartinVerner ZdeněkKičura TomášMann HeřmanOreská SabínaSvobodová KristinaKropáčková TerezaTomčík MichalUkropec JozefUkropcová BarbaraVencovský Jiří - Tumor-associated endothelial cells (TAECs) are integral components of the clear cell renal cell carcinoma (ccRCC) microenvironment, but their gene expression-based prognostic value and functional relevance remain to be defined. - Source: PubMed
Publication date: 2026/07/02
Liu QingCao WenxingHao Zhouhua