SERPINA3 monoclonal antibody, clone 802
- Known as:
- SERPINA3 mab (anti-), clonality 802
- Catalog number:
- MAB4113
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- SERPINA3 monoclonal antibody clone 802
Related genes to: SERPINA3 monoclonal antibody, clone 802
- 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 monoclonal antibody, clone 802
Related articles to: SERPINA3 monoclonal antibody, clone 802
- 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 - Understanding the molecular mechanisms of autism spectrum disorder (ASD) and its psychiatric comorbidities, including bipolar disorder (BD), is pivotal for uncovering pathways that shape neurodevelopmental trajectories and clinical heterogeneity. We aimed to identify ASD-specific gene-expression signatures and disrupted biological processes in prefrontal cortex, contrasting them with those observed in BD. - Source: PubMed
Publication date: 2026/08/04
Marmontel PedroRabelo-da-Ponte Francisco DiegoKapczinski FlávioGottfried Carmem - Neonatal calf health critically depends on successful passive transfer of immunity (PTI) via colostrum. Although PTI is routinely assessed by serum IgG concentration, associated systemic proteomic responses remain poorly defined. This study aimed to relate distinct PTI categories to neonatal calf serum proteomes and to evaluate colostrum proteomes to identify proteins influencing passive transfer success. Forty Holstein cow-calf pairs were enrolled. Calf serum was collected before colostrum feeding (0 h) and at 48 h. Serum IgG was quantified by ELISA, and calves were classified at 48 h as failed (FPTI, <1000 mg/dL, n = 11), adequate (APTI, 1000-2000 mg/dL, n = 11), or excellent (EPTI, >2000 mg/dL, n = 18). For proteomic analyses, five calves were purposefully selected in each group; serum samples were pooled by PTI group and time point, and colostrum samples by PTI group, then analyzed by LC-MS/MS in DIA mode. Proteomics identified 54 proteins in colostrum and 80 in serum, 27 of which were shared between matrices. Post-colostrum intake, 21 (FPTI), 5 (APTI), and 30 (EPTI) serum proteins changed significantly from 0 to 48 h. In EPTI calves, haptoglobin (Hp) (51.10-fold) and pigment epithelium-derived factor (PEDF) (27.24-fold) showed the strongest upregulation. At 48 h, lipopolysaccharide-binding protein (LBP) and haemoglobin subunit epsilon (Hb-ε) were lower in EPTI, whereas PEDF, polymeric immunoglobulin receptor (PIGR), and SERPINA3-6 were higher, consistent with coordinated activation of acute-phase, mucosal/transport, and protease-antiprotease pathways. These findings indicate that PTI involves coordinated proteomic changes beyond IgG alone and highlight candidate biomarkers of successful passive immunity in neonatal calves. - Source: PubMed
Publication date: 2026/07/17
Kaçar YiğitTopal OnurMecitoğlu ZaferSağlam NezaketFthenakis George CBatmaz Hasan - Maternal obesity is a well-established risk factor for preeclampsia; however, whether increased maternal BMI is associated with biologically distinct subtypes of this disorder remains unknown. - Source: PubMed
Publication date: 2026/07/14
Duehring Jasmin AYu Peter TDeihl Tiffany EFlyer ZoeSchomberg John P - Preeclampsia (PE) is a severe pregnancy-specific complication characterized by new-onset hypertension and proteinuria after 20 weeks of gestation, which can cause multi-organ damage and life-threatening outcomes for both mothers and foetuses. Its pathogenesis remains incompletely elucidated, with placental dysfunction widely recognized as a core pathogenic factor. This study integrated multiple placental transcriptome and single-cell sequencing datasets from the Gene Expression Omnibus (GEO) database, employing a multi-dimensional bioinformatics approach - including differential expression analysis, Weighted Gene Co-expression Network Analysis (WGCNA), machine learning, molecular subtype clustering, single-cell resolution analysis, and intercellular communication analysis - to systematically identify PE-related key genes, construct a diagnostic model, define molecular subtypes, and explore potential molecular mechanisms. Results showed 10 differentially expressed genes (DEGs) were identified in PE placental tissues; WGCNA pinpointed the turquoise module as the core PE-associated module. Further screening using 11 machine learning algorithms identified 9 feature genes with high diagnostic value (DDR1, DIO2, FSTL3, HK2, HTRA4, LEP, SERPINA3, TMEM45A, TREM1). A diagnostic model built with the 'Stepglm[forward]' algorithm exhibited excellent performance in both training and validation sets (average AUC = 0.865). Molecular subtype analysis classified PE samples into two subtypes (C1, C2) with significantly distinct immune infiltration profiles, where the C1 subtype showed higher immune cell infiltration. Single-cell analysis identified 11 cell types in PE placental tissue and highlighted TMEM45A as a key DEG. Intercellular communication analysis revealed the VEGF signalling pathway as the core driver of abnormal cellular crosstalk in PE, primarily mediating signal transduction between villous cytotrophoblast cells (VCT), extravillous trophoblast cells (EVT), and endothelial cells. Hypoxia scoring analysis demonstrated significantly higher hypoxia levels in the PE group compared to normal controls, with TMEM45A expression positively correlated with hypoxia scores. This study provides novel insights into the molecular pathogenesis of PE and offers potential biomarkers and a theoretical basis for its early diagnosis and targeted therapy. - Source: PubMed
Publication date: 2026/07/20
Li NiTian LinWei Haiyun