Sheep Leukocyte elastase inhibitor(SERPINB1) ELISA kit
- Known as:
- Sheep Leukocyte elastase suppressor(SERPINB1) Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- e14l0337
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Blue gene shanghai
- Gene target:
- Sheep Leukocyte elastase inhibitor(SERPINB1) ELISA kit
Related genes to: Sheep Leukocyte elastase inhibitor(SERPINB1) ELISA kit
- Gene:
- SERPINB1 NIH gene
- Name:
- serpin family B member 1
- Previous symbol:
- ELANH2
- Synonyms:
- EI, PI2, anti-elastase
- Chromosome:
- 6p25.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-07-27
- Date modifiied:
- 2016-04-06
Related products to: Sheep Leukocyte elastase inhibitor(SERPINB1) ELISA kit
Related articles to: Sheep Leukocyte elastase inhibitor(SERPINB1) ELISA kit
- Multiple sclerosis (MS) is a severe neuroinflammatory disease causing substantial long-term disability. Strong epidemiologic evidence links Epstein-Barr virus (EBV) exposure with MS risk, but genetic evidence for immune target prioritization in EBV-related phenotypes remains limited. - Source: PubMed
Publication date: 2026/08/05
Zhou YixiangHuang XindiShe XiaoHao QinMi ZhikuanYang Yanling - Chronic inflammatory lung diseases are associated with elevated levels of neutrophil elastase (NE), leading to epithelial damage and dysregulated cellular responses. However, the molecular mechanisms underlying NE-mediated disruption of epithelial anti-protease defenses, including the regulation of SERPINB1, remain poorly defined. In this study, we investigated NE-induced responses in bronchial epithelial cells cultured at air-liquid interface (ALI) focusing on epithelial cell death, inflammation, and SERPINB1 dynamics. NE exposure induced dose- and time-dependent cytotoxicity, accompanied by morphological alterations, mitochondrial membrane depolarization, and modest changes in caspase-3, -8, and -9 activity. In ALI cultures, NE was applied either apically, basolaterally or to both compartments simultaneously to evaluate exposure-side-dependent epithelial responses. NE differentially modulated apoptosis-related gene expression, including changes in BCL2, BAX, CASP3, CASP8, CASP9, PARP1, and AIF, depending on NE concentration and exposure side. Cytokine profiling revealed dose-, exposure-side-, and sampling-compartment-dependent changes in IL-6, IL-8, and GM-CSF secretion. Importantly, SERPINB1 expression was markedly reduced at both mRNA and protein levels, while domain-specific immunofluorescence suggested altered SERPINB1 localization and epitope accessibility, suggesting functional alterations beyond transcriptional loss. siRNA-mediated SERPINB1 knockdown further modified NE-associated apoptosis-related gene expression, supporting a functional link between NE exposure and epithelial SERPINB1 regulation. Collectively, these findings establish the NE-SERPINB1 axis as a critical determinant of epithelial cell fate, contributing to epithelial apoptosis, inflammatory mediator release, and protease-antiprotease imbalance. This study provides a systematic analysis of dose- and exposure-side-dependent epithelial responses to NE under ALI culture conditions. Our results highlight the NE-SERPINB1 axis as a contributor to epithelial dysfunction in chronic airway inflammation and support the exploration of SERPINB1-modulating strategies for preserving epithelial integrity and mitigating neutrophil-driven pathology in lung diseases. - Source: PubMed
Publication date: 2026/07/04
Kilic BusraAkel Bilgic HayriyeKaraaslan Cagatay - Septic shock is a life-threatening syndrome characterized by immune dysregulation, oxidative injury, and high mortality. To identify candidate regulators linking immunity and ferroptosis in septic shock, we integrated expression quantitative trait loci (eQTL)-based Mendelian randomization (MR) with transcriptomic datasets from septic shock patients and controls. Differentially expressed genes overlapping with MR-prioritized genes were further evaluated using 113 machine-learning models, among which the glmBoost plus elastic net model (alpha = 0.9) showed strong discriminatory performance, with area under the curve (AUC) values of 0.999 in GSE26378, 0.980 in GSE26440, and 0.987 in the meta-cohort. The final model retained four risk genes, SERPINB1, DDAH2, SLC22A4, and CEACAM6. Among them, SLC22A4/OCTN1, an ergothioneine transporter, was associated with neutrophil-related immune features and better survival-related outcomes, whereas CEACAM6 showed a distinct pattern associated with immune dysregulation. Protein-ligand docking predicted potential interactions between candidate compounds and selected target proteins. In neutrophil-based validation experiments, SLC22A4 perturbation altered inflammatory cytokine production, STING-associated signaling readouts, and ferroptosis-related markers. Additional transporter-related assays showed that SLC22A4 knockdown reduced intracellular ergothioneine accumulation and that ergothioneine supplementation partially rescued erastin-induced viability loss and lipid ROS accumulation. In a cecal ligation and puncture (CLP) model, D-carnitine hydrochloride, STING-IN-5, and Keap1-Nrf2-IN-9 reshaped inflammatory cytokine responses and were associated with partial attenuation of septic lung injury. These findings suggest that SLC22A4 may represent a candidate regulator connecting immune remodeling with ferroptosis-associated dysfunction in septic shock; however, independent cohort validation, direct in vivo target-engagement studies, and further mechanistic analyses are required before therapeutic translation. - Source: PubMed
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