SERPINA3 Mouse Monoclonal Antibody
- Known as:
- SERPINA3 Mouse Monoclonal Antibody
- Catalog number:
- ANG-000012-M01
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- SERPINA3 Mouse Monoclonal Antibody
Related genes to: SERPINA3 Mouse Monoclonal Antibody
- 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 Mouse Monoclonal Antibody
Related articles to: SERPINA3 Mouse Monoclonal Antibody
- Rheumatoid Arthritis (RA) is a Prevalent Autoimmune Disorder Affecting Millions of People Worldwide. A Thorough Understanding of Its Clinical and Pathological Features Is Essential to Improve Patient Outcomes. - Source: PubMed
Zhao YangLi YuanQi MengXu JunhuaJi FengweiKan YanKong Chunyu - 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 - Diagnostic evaluation of suspected neuromyelitis optica spectrum disorder (NMOSD) integrates AQP4-IgG testing, clinical assessment, neuroimaging, and exclusion of alternative inflammatory demyelinating disorders; nevertheless, some patients remain diagnostically unresolved or may be misclassified as multiple sclerosis (MS) or other disorders. This single-center retrospective exploratory study analyzed quantitative serum proteomics from 20 patients with MS and 20 with NMOSD. Proteins meeting nominal < 0.05 together with prespecified fold-change criteria were considered exploratory candidates. VWF, PPBP, and SERPINA3 were subsequently assessed by ELISA in a separate, non-overlapping cohort from the same center, together with routine hematological variables. Among 261 protein entries, 34 met the exploratory nominal threshold and fold-change criteria, but none remained significant after Benjamini-Hochberg correction (lowest q = 0.0734). VWF and PPBP showed no significant differences across the four validation groups. SERPINA3 differed across groups (Kruskal-Wallis H = 44.982, = 9.34 × 10) and was higher in NMOSD than in MS, TBI, and HCs after Holm adjustment (adjusted = 0.036, 1.49 × 10, and 1.13 × 10, respectively). In the full ELISA cohort, the AUC was 0.928 for NMOSD versus HC and 0.800 for NMOSD versus MS. In a post hoc sensitivity analysis excluding participants with preceding infection, the NMOSD-MS separation was attenuated. In smaller complete-case analyses, adding an additional laboratory variable to SERPINA3 did not significantly improve apparent discrimination. SERPINA3 is therefore an exploratory adjunctive serum biomarker candidate rather than a stand-alone diagnostic test; prospective external validation in clinically representative cohorts is required. - Source: PubMed
Publication date: 2026/08/20
Xu TingHan BingqingZheng GuanghuiJiang WencanZhang HanyuZhang Guojun - Murine serine protease inhibitor clade A member 3N (SERPINA3N) and its human homolog SERPINA3 are injury-associated molecules induced in virtually all neurological conditions including ischemic stroke. Clinically, SERPINA3 is elevated in stroke patients, correlating with severe brain pathology and worse neurological outcomes. Yet, the exact cellular sources and therapeutic value of SERPINA3N/SERPINA3 in the ischemic brain remain elusive. Here, we report that oligodendrocytes are the major sources of SERPINA3/SERPINA3N and that SERPINA3N exerts neurotoxic effects in experimental cerebral ischemia. Given SERPINA3N's secretory nature, we used knock-in Serpina3n-tdTom reporter mice to define its temporospatial evolution. The tdTom signal was barely detectable by day1 but gradually increased from day 3 through day 7 following cerebral ischemia. The majority of tdTom cells were identified as oligodendrocytes and astrocytes with fewer found in neurons or microglia. This cellular identity was corroborated by meta-analysis of single-cell transcriptomics datasets and human ischemic stroke brain data. Antagonizing SERPINA3N attenuated blood-brain barrier disruption, neuroinflammation, and neuronal damage and improved neurological function in a mouse model of cerebral ischemia. These findings resolve a longstanding debate regarding the cellular origins of SERPINA3N, identifying oligodendrocytes as its major source. Our studies highlight SERPINA3N antagonism as a possible therapeutic intervention for ischemic stroke, providing new insights for precision therapies that target oligodendroglia- or astroglia-specific SERPINA3N. - Source: PubMed
Publication date: 2026/07/29
Park JoohyunKim Hyun KyuBarman BhabotoshSobel Raymond AYenari Midori AGuo Fuzheng - Cirrhosis, accounting for 2.4% of global mortality in 2019, represents a leading cause of death in chronic liver disease. Hepatic encephalopathy (HE), a decompensated complication of cirrhosis, is associated with a median survival of only 0.92 years post-diagnosis. Current screening methods relying on neuropsychological tests (e.g., Psychometric Hepatic Encephalopathy Score, PHES) have limitations such as time-consuming procedures and subjective interpretation, potentially delaying diagnosis. To address this, we integrated four cirrhotic transcriptomic cohorts (GSE41919, GSE57193, GSE139602, and GSE15654) and employed an integrated algorithm (LASSO [Least Absolute Shrinkage and Selection Operator]-RFE [Recursive Feature Elimination]-random forest) to identify HE-specific biomarker genes. Ultimately, we developed an HE risk-prediction system centered on eight HE-specific marker genes, namely, , , , , , , and . Based on these genes, an XGBoost (eXtreme Gradient Boosting)-based HE risk stratification model was constructed, and SHAP (SHapley Additive exPlanations) analysis was further introduced to address the "black-box" limitation of conventional machine learning models and to improve the interpretability. The finalized eight-gene system enables accurate, efficient, and interpretable HE risk assessment in patients with cirrhosis. Functional characterization through gene set enrichment analysis and structural equation modeling further revealed that these marker genes converge on four interconnected biological processes, namely, metabolic homeostasis, synaptic and neural transmission, immune inflammatory signaling, and hepatic detoxification, which collectively reflect the gut-liver-brain axis disruption central to HE pathogenesis. This dual-model system, incorporating both cirrhosis progression and survival prognosis, provides a reliable and clinically applicable tool for early HE risk warning and stratification, reducing the limitations of traditional neuropsychological screening and offering a translational foundation for timely intervention and prognostic optimization in high-risk cirrhotic patients. - Source: PubMed
Publication date: 2026/08/01
Lan YuanfengZhao TianXu YingYe Haihong