Ask about this productRelated genes to: SERPINF2 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: SERPINF2 antibody
Related articles to: SERPINF2 antibody
- Delayed postoperative hemorrhage (DEPOH) is recognized in sighthound breeds and has been associated with a SERPINF2 c.605C>T variant that affects alpha-2-antiplasmin, an important inhibitor of fibrinolysis. The distribution of this variant among dogs in Japan has not been investigated. To determine the frequency of the SERPINF2 c.605C>T variant in dogs presented to a single referral hospital in Japan. Genomic DNA was extracted from peripheral blood of dogs presented to the Animal Medical Center of Nihon University between July 2021 and October 2022. Genotyping of SERPINF2 c.605C>T variant was performed by real-time PCR using a TaqMan minor groove binder SNP genotyping assay. Adequate amplification was obtained in 433 of 436 samples. Homozygous variant genotypes (T/T) were detected in one Italian Greyhound, one Whippet, and two Shiba Inu dogs. Heterozygous genotypes (C/T) were detected in Saluki, Italian Greyhound, Shiba Inu, French Bulldog, mixed-breed dog, Boston Terrier, Jack Russell Terrier, and Chihuahua. Among non-sighthound breeds, Shiba Inu dogs had the highest observed variant allele frequency in this cohort (0.25). The DEPOH-associated SERPINF2 c.605C>T variant was detected in both sighthound and non-sighthound dogs in this Japanese referral-hospital cohort. The relatively high allele frequency observed in Shiba Inu dogs warrants further multicenter studies evaluating variant frequency and its relationship with clinical DEPOH. - Source: PubMed
Publication date: 2026/07/22
Maruyama HaruhikoOzaki NanakoKato KumiNishimura Saki - Cetaceans face the risk of thromboembolism due to diving and decompression responses. However, cetaceans maintain normal blood circulation. This study explores the molecular mechanisms cetaceans use to mitigate diving-associated hemostatic challenges during diving. Forty-six species were analyzed, including 18 cetaceans, 9 artiodactyls, and 19 other terrestrial mammals. Thirty-nine anticoagulant genes and proteins were examined, identifying 6 genes (ANXA2, ANXA5, FGA, FGB, PLAUR, and PLG) with conserved evolution, 4 genes (ANXA2, PDGFB, SH2B3, THBS1) with positive selection, and 12 proteins (APOH, FGA, FGB, FGG, GP1BA, PLAU, PRKCD, PRKG1, SERPINF2, SERPING1, TMPRSS6, and TMX1) with specific amino acid sites in cetaceans. Ancestral state reconstruction revealed independent evolution of deep diving behavior in different cetacean lineages, particularly within Odontoceti. Correlation analysis linked the evolution of the APOE gene with diving depth, suggesting its role in diving adaptation. These analyses suggest that cetaceans may help reduce the risk of thrombosis during diving by lowering platelet activity, enhancing fibrinolysis, and modulating the coagulation cascade. These analyses suggest that cetaceans may mitigate diving-associated thrombotic risk by modulating platelet activity, fibrinolysis, and the coagulation cascade. Overall, this study identifies candidate anticoagulant-related genes and amino acid substitutions for future functional validation of hemostatic adaptation in cetaceans. - Source: PubMed
Publication date: 2026/07/06
Lv WenjunCao LiZhang YaXu ShixiaRen Wenhua - Renal transplant patients (RTPs) receiving immunomodulatory therapy are at increased risk of severe complications from COVID-19 and other infections. This study aimed to identify immune and proteomic biomarkers associated with COVID-19 in RTPs to improve disease characterization and support future diagnostic and therapeutic strategies. - Source: PubMed
Publication date: 2026/06/12
Alaiya AyodeleAl-Mozaini MahaShinwari ZakiaAlzayed AbdulazizAlsharif IbtihajAllam RababBakheet RazanAlharbi LaylaAlotaibi Fahad OjabIdris JumanaObeid Dalia AAlshukairi AbeerMárquez-Méndez MarcelaCerda-Flores Ricardo MAlmojalli Hamad A - 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. Human CTCs were challenged with cigarette smoke extract (CSE) to model oxidative stress-driven PE pathology. Two paradigms were tested: (1) prophylactic aspirin (4 and 40 µg/mL) before and/or flanking the CSE, and (2) therapeutic aspirin after the CSE challenge. The EVs were isolated via ultracentrifugation and size-exclusion chromatography, characterized by nanoparticle tracking and immunoblotting, and profiled by quantitative mass spectrometry. A network pathway analysis and machine learning biomarker selection defined the EV-encoded molecular states. The CTC-derived EVs from the CSE-exposed cells carried a PE-like proteomic signature marked by suppressed VEGF/ECM remodeling, activated TNF-p53 apoptotic signaling, and heightened inflammation. Prophylactic low-dose aspirin shifted the EV cargo toward an EV-encoded signature consistent with preserved angiogenic potential (enrichment of VEGFA, COL1A1, and MMP14) and predicted attenuation of apoptotic and NF-κB pathway activity by an Ingenuity Pathway Analysis. High-dose aspirin produced broad transcriptional suppression without an accompanying pro-angiogenic EV signature. Therapeutic (post-injury) aspirin partially attenuated the injury-associated EV cargo but did not restore the angiogenic EV signature. An exploratory machine learning analysis of EV proteomes identified a candidate prophylactic biomarker panel anchored by HSPA8, SERPINF2, COL4A1, and PLOD1, mapped to the predicted angiogenic recovery and redox-balance pathways. These EV cargo readouts represent the predicted molecular states and require functional validation before clinical interpretation. The CTC-derived EV proteomic signatures capture the dose- and timing-dependent aspirin effects in this in vitro CTC model, positioning the chorion as a candidate pharmacological "secondary responder" favoring cellular resilience over classical anti-inflammatory suppression. As an exploratory hypothesis-generating study, EV-based molecular profiling could provide a foundation for future investigations aimed at stratifying aspirin responders from non-responders, although clinical validation in maternal plasma cohorts will be required before any translational application. - Source: PubMed
Publication date: 2026/05/29
Mahajan VineetKumar AwanitJacob JeenaCostantine Maged MRichardson Lauren SUrrabaz-Garza RheannaAmabebe EmmanuelTantengco Ourlad Alzeus GKammala Ananth KumarMenon Ramkumar - 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: 2026/06/08
Mathavan AkshayMathavan AkashKrekora UrszulaMagar StephenAl-Nazer MajedAtaya AliMathew CarolHarris Neil SRajasekhar Anita