Ask about this productRelated genes to: A2AP antibody
- Gene:
- SERPINF2 NIH gene
- Name:
- serpin family F member 2
- Previous symbol:
- PLI
- Synonyms:
- API, ALPHA-2-PI, A2AP, AAP
- Chromosome:
- 17p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1989-04-14
- Date modifiied:
- 2019-04-23
Related products to: A2AP antibody
Related articles to: A2AP antibody
- Alpha-2 antiplasmin (α2AP) deficiency is a rare fibrinolytic disorder characterized by unregulated plasmin activity and premature clot breakdown. Mechanistically, α2AP restrains fibrinolysis by (i) forming a covalent serpin complex with plasmin, (ii) blocking plasminogen binding to fibrin, and (iii) undergoing factor XIIIa-mediated cross-linking into fibrin to harden clots against local lysis. We describe a woman with decades of delayed postoperative bleeding, transfusion dependence, and a presumed diagnosis of von Willebrand disease, ultimately found to have congenital α2AP deficiency. Her evaluation showed normal coagulation studies, platelet function, and von Willebrand factor assays, with persistently low α2AP activity and a homozygous SERPINF2 variant confirming the diagnosis. Standard hemostatic panels may fail to detect α2AP deficiency, and testing with functional activity assays or genetic analysis is required. This case highlights diagnostic pitfalls and underscores the importance of considering fibrinolytic disorders in patients with unexplained or delayed bleeding. - Source: PubMed
Publication date: 2026/06/09
Mathavan AkshayMathavan AkashKrekora UrszulaMagar StephenAl-Nazer MajedAtaya AliMathew CarolHarris Neil SRajasekhar Anita - As the natural hosts of avian influenza virus (AIV), wild birds generally exhibit a more tolerant immune response to AIV infection compared to domestic poultry. However, the underlying mechanisms remain incompletely understood, partly due to limited access to wildlife biological samples imposed by animal protection principles. To investigate these differential immune responses, we established a peripheral blood mononuclear cells (PBMCs) infection platform. PBMCs from domestic chickens and swan geese were infected with H9N2 AIV, and label-free quantitative comparative proteomics was performed to identify differentially expressed proteins (DEPs) between the two species, aiming to uncover potential host antiviral factors. Proteomic analysis revealed that chicken PBMCs showed marked activation of antiviral defense and inflammatory pathways, accompanied by upregulation of oxidative stress-related pathways. In contrast, swan goose PBMCs predominantly activated pathways associated with cellular integrity maintenance, metabolic homeostasis, and RNA surveillance. Subsequently, 12 DEP candidates with high expression fold-changes in swan goose PBMCs were selected and expressed in DF-1 cells to evaluate their antiviral activities. Among these, only SERPINF2, a member of the serine protease inhibitor family, significantly inhibited H9N2 AIV replication in DF-1 cells. Mechanistically, SERPINF2 suppressed viral replication by specifically inhibiting the cleavage of the viral hemagglutinin (HA) protein, thereby reducing the production of infectious progeny virions. This study reveals distinct immune response patterns to H9N2 AIV infection in chickens and swan geese, and identifies SERPINF2 as a novel restriction factor against H9N2 AIV, providing new insights into the antiviral mechanisms in natural AIV hosts. - Source: PubMed
Publication date: 2026/05/29
Li FangbingRen ChenyangLiu WanlinYu XinYu JindanMa YunfengFeng YaliZhang Ying - Biological mechanisms underlying heterogeneous antipsychotic response in schizophrenia remain incompletely understood. In this exploratory cross-sectional study, we applied deep data-independent acquisition LC-MS/MS plasma proteomics to 56 adults initially enrolled (14 per group), including healthy controls and patients meeting TRRIP criteria for treatment-sensitive (TSS), treatment-resistant (TRS), and ultra-treatment-resistant schizophrenia (UTRS). Following proteomic quality control and exclusion of outliers, 52 individuals comprised the final analytical cohort. Proteomic data were analyzed using a layered strategy integrating covariate adjustment, variance partitioning, mediation analysis, monotonicity filtering, LASSO stability assessment, and redundancy reduction. More than 1400 plasma proteins were quantified; 450 differed across groups before adjustment, and 310 reviewed proteins remained significant after covariate modeling. A sensitivity-associated profile distinguishing TSS from controls (CRP, CCDC62, FBXW7, GULP1, CALD1, COPS6) was consistent with lower inflammatory tone and relative preservation of proteostatic and cytoskeletal regulation. In contrast, a resistance-associated profile separating TRS/UTRS from TSS (SHROOM1, MYH7, ABR, EZR, SERPINF2) converged on cytoskeletal organization, actin-membrane dynamics, and extracellular regulatory processes. Directionally concordant but quantitatively amplified changes were observed in UTRS relative to TRS, although multivariate separation between resistant subgroups was limited after full covariate adjustment. Several proteins enriched in resistant groups corresponded to intracellular or nuclear factors rarely detected in plasma and require cautious interpretation. Overall, these findings are compatible with a progression-like molecular pattern in which treatment sensitivity and resistance may reflect shifts in cellular adaptability and structural regulation. Replication in larger and longitudinal cohorts is required. - Source: PubMed
Publication date: 2026/04/27
de Oliveira Caio AndradeSoares Michelle Verde Ramode Pinho Carolina Saraiva NunesPinto Joel PorfírioFrota Annyta FernandesMoreira Ana Cristina de OliveiraSilva Maria Francilene SouzaBatista Tiago de OliveiraHallak Jaime Eduardo CecilioSheheryar SheheryarMoura Arlindo De Alencar Araripe NoronhaSanders Lia Lira OGallo Margareth Borges Coutinhode Sousa Felipe DomingosMacedo Danielle S - Contrast-induced acute kidney injury (CI-AKI) is a major cause of hospital-acquired AKI, but its molecular pathogenesis remains incompletely understood. In this study, we used quantitative 4D proteomics, integrating ion mass-to-charge ratio (m/z), retention time, ion intensity, and ion mobility, to profile renal tissues from a novel rat CI-AKI model based on renal venous congestion and contrast exposure, with sham-operated rats as controls. Differentially expressed proteins were identified and analyzed using pathway enrichment and protein-protein interaction (PPI) network approaches, followed by experimental validation. Using nominal screening criteria (|log2FC| ≥ 1.5 and < 0.05), we identified 180 candidate differentially expressed proteins, including 92 upregulated and 88 downregulated proteins. Pathway-level analyses showed coordinated upregulation of complement-related proteins, including C3/C5 convertase-related components and terminal pathway proteins, such as C9, together with a C4 isoform annotated as C4a in the reference database. Coagulation and fibrinolysis pathways were also markedly altered, including fibrinogen chains (FGA, FGB, FGG), PLAU, SERPINA1, and SERPINF2. In contrast, proteins associated with AMPK and MAPK signaling (including HNF4α, PRKAA2, PRKAB1, and MAP2K3) were reduced. These pathway-level changes were supported by RT-qPCR and immunohistochemical analyses. Collectively, our findings support a multidimensional injury network in rat CI-AKI involving complement activation, coagulation-fibrinolysis dysregulation, and impaired metabolic/stress-response signaling, and provide a proteomic resource for future mechanistic and translational studies. - Source: PubMed
Publication date: 2026/04/14
Yang QiangSun LimingZhang ZhijianYan ZhixinZhang JianHu JiachangDing Xiaoqiang - Low-dose aspirin (LDA) reduces preeclampsia (PE) risk by up to 40%, yet its molecular effects on chorion trophoblast cells (CTCs) a fetal membrane lineage at the feto-maternal interface remain obscure. CTCs form a structural and immunoregulatory barrier whose dysfunction drives inflammation-associated membrane pathology in PE. Extracellular vesicles (EVs) released by CTCs may encode cellular stress and adaptation states, offering a molecular window into aspirin's timing-dependent effects on PE risk modification. - Source: PubMed
Publication date: 2026/03/10
Mahajan VineetKumar AwanitJacob JeenaConstantine MagedRichardson Lauren SUrrabaz-Garza RheannaAmabebe EmmanuelTantengco Ourlad AKammala Ananth KMenon Ramkumar