SERPINA3 Antibody (Center)
- Known as:
- SERPINA3 Antibody (Center)
- Catalog number:
- AP7314c
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- SERPINA3 Antibody (Center)
Related genes to: SERPINA3 Antibody (Center)
- Gene:
- SERPINA3 NIH gene
- Name:
- serpin family A member 3
- Previous symbol:
- AACT
- Synonyms:
- ACT
- Chromosome:
- 14q32.13
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-04
Related products to: SERPINA3 Antibody (Center)
Related articles to: SERPINA3 Antibody (Center)
- Sinensetin (SIN) is a natural flavonoid with potential anti‑inflammatory effects. This study investigated whether SIN ameliorates osteoarthritis (OA) and explored its underlying mechanisms. In vitro, SIN (0.05-1 μg/mL) protected human OA chondrocytes from IL‑1β‑induced viability loss. Transcriptome sequencing and molecular docking identified SERPINA3 as a candidate target of SIN. SIN reduced the expression of NLRP3, GSDMD, and ASC, inhibited pyroptotic morphology, decreased TUNEL‑positive cells and LDH release, and lowered IL‑1β and IL‑18 secretion in IL‑1β‑treated chondrocytes. Knockdown of SERPINA3 reversed these effects, suggesting that SIN acts through SERPINA3 to inhibit the NLRP3 inflammasome. In a rat DMM‑induced OA model, SIN (20 mg/kg/day for 6 weeks) alleviated pain, reduced OARSI scores, improved cartilage matrix staining (Safranin O, Masson's trichrome), attenuated synovial hyperplasia and posterior capsule adhesions, and decreased plasma IL‑1β and IL‑18 levels. Western blot of rat cartilage confirmed that SIN suppressed GSDMD and NLRP3 expression. These results indicate that SIN ameliorates OA progression by inhibiting SERPINA3‑mediated NF‑κB/NLRP3‑driven chondrocyte pyroptosis. SIN may be a potential therapeutic candidate for OA. - Source: PubMed
Publication date: 2026/10/07
Liu ZhendongLiu RuizhouYue HongweiLiu PeilaiWang Rui - Heart failure (HF) is a leading cause of global morbidity and mortality, yet the crosstalk between energy metabolism reprogramming and myocardial fibrosis remains poorly understood. This study aimed to identify glycolysis- and myocardial fibrosis-related diagnostic biomarkers in HF through integrative bioinformatics analysis. - Source: PubMed
Publication date: 2026/09/22
Yang LinLiu BingQiu ShuangZhang YimengTa NaLiu Yanxia - Ductal carcinoma in situ (DCIS) is a non-invasive precursor of invasive ductal carcinoma (IDC), yet the biological mechanisms underlying the transition from DCIS to IDC remain incompletely understood. Here, we integrate spatial transcriptomics, single-cell RNA sequencing, and single-cell DNA sequencing on coexisting DCIS and IDC samples to characterize cellular and microenvironmental alterations. Integrated analyses reveal differential molecular characterizations between coexisting DCIS and IDC and identify candidate genes (MGP, PLAT, and SERPINA3) potentially limiting the progression from DCIS to IDC. Malignant epithelial meta-programs (MPs) delineate distinct transcriptional states, with development-associated MP1 enriched in DCIS and cell cycle-related MP5 enriched in IDC. Further analysis reveals varied microenvironmental features in DCIS and IDC, with invasion-associated Mph_SPP1 and development-associated iCAFs_HOPX enriched in DCIS, while immunosuppressive Mph_PRDM1 and metabolism-related tCAFs_BNIP3 predominate in IDC. We then construct a machine learning model to identify DCIS at high risk of progression, which is externally validated across independent bulk RNA-sequencing cohorts (mean AUC = 0.903). Collectively, this study provides an integrative framework for understanding the molecular and spatial features that distinguish DCIS from IDC, with the potential to inform more precise risk stratification and clinical management for DCIS progression. - Source: PubMed
Publication date: 2026/09/27
Zhang NingWan TongZhang SiyueJiang YunzhenSu PengLiu JixinChen ZhitongHao JieWang HaoyuChen BingZhao WenjingWang LijuanXing TaoZhang QihuangSchmitz UlfDing ZhiyongCrosetto NicolaLiu BingqiangYang Qifeng - To examine the main adverse cardiovascular events that occur in individuals who have had an acute ST-segment elevation myocardial infarction (STEMI) after receiving percutaneous coronary intervention (PCI), such as serum C-type lectin domain family member 2 (CLEC2), serine protease inhibitor family member A3 (SERPINA3), and high-sensitivity C-reactive protein/albumin (hs-CRP/ALB) levels. - Source: PubMed
Ma YuncongFang SuxiaLiu ShashaJiang Zhencong - The molecular mechanisms linking vascular aging (VA) and heart failure (HF) remain elusive, hindering therapeutic strategies for their comorbidity. This study aimed to identify key biomarkers and pathways potentially involved in VA-HF synergy using integrative computational approaches. - Source: PubMed
Publication date: 2026/09/15
Li JinzeZhou GuitingWang QiaochuSong ZhixuanLiu JiantaoShen ChangzaoLuo ChuanjinWang Dawei