Recombinant Human Secreted Phospholipase A2-V PLA2G5
- Known as:
- Recombinant Human Secreted Phospholipase A2-V PLA2G5
- Catalog number:
- enz-328
- Product Quantity:
- 2
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- Recombinant Human Secreted Phospholipase A2- PLA2G5
Related genes to: Recombinant Human Secreted Phospholipase A2-V PLA2G5
- Gene:
- PLA2G5 NIH gene
- Name:
- phospholipase A2 group V
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1p36.13
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-30
- Date modifiied:
- 2016-10-05
Related products to: Recombinant Human Secreted Phospholipase A2-V PLA2G5
Related articles to: Recombinant Human Secreted Phospholipase A2-V PLA2G5
- Despite extensive advances in understanding sepsis pathophysiology, treatment outcomes have not substantially improved. In this issue, Takahama and colleagues identified phospholipase A2 Group V (PLA2G5) as a contributor to sepsis lethality in mouse models of endotoxemia and sepsis. Whole-mouse spatial profiling generated bodywide maps of systemic inflammation and uncovered intestinal goblet cells as a source of pathogenic PLA2G5. Pairs of inflammatory cytokines (TNF and IFN-γ, or TNF and IL-18) induced PLA2G5 expression in goblet cells. Mechanistically, circulating PLA2G5 triggered intravascular hemolysis through its lipolytic activity on erythrocyte membranes and contributed to organ failure and death. PLA2G5's deleterious effects were blocked by specific antibodies and were absent in Pla2g5-deficient mice. In humans with bacterial or fungal sepsis or severe COVID-19, plasma PLA2G5 levels were elevated and predicted disease severity. This discovery highlights the contribution of hemolysis to sepsis, suggesting that PLA2G5 inhibitors, hemoglobin, or heme antagonists could represent valuable therapeutic tools. - Source: PubMed
Publication date: 2026/05/01
Cavaillon Jean-Marc - Sepsis is a systemic response to infection with life-threatening consequences such as hemolysis, a predictor of mortality risks for the disease. Here, by measuring organism-wide changes in gene expression, we discovered that the secreted phospholipase PLA2G5 is induced in colon cell types during sepsis. The genetic deletion of Pla2g5 and treatment with a PLA2G5 antibody were both associated with protection from lethal sepsis. Treatment with a PLA2G5 antibody during sepsis was associated with increased splenic red pulp macrophages and improved iron homeostasis, linking PLA2G5 to red blood cell homeostasis during sepsis. Mechanistically, bloodborne PLA2G5 led to intravascular hemolysis through its lipolytic activity on red blood cell membranes. In humans with sepsis due to bacterial, fungal, or viral infections, the serum level of PLA2G5 was elevated and predictive of disease severity and mortality. We conclude that sepsis corrupts PLA2G5 into becoming an intravascular hemolytic factor which is toxic for host red blood cells. - Source: PubMed
Publication date: 2026/05/01
Takahama MichihiroWolfe Krysta SRichey GabriellaPlaster MadisonCzapar AnnaHernandez FabianCipurko DenisUeda TatsukiMiki YoshimiNagasaki YukiTaketomi YoshitakaSaitoh TatsuyaKawamoto TadafumiDudek Steven MMurakami MakotoChevrier Nicolas - Low-grade gliomas(LGGs) show significant clinical and molecular heterogeneity, complicating progression prediction with conventional indicators. Metabolic reprogramming, a cancer hallmark, is linked to immune microenvironment remodeling, yet its role in LGG prognostic modeling remains underexplored. This study aims to develop a robust metabolism-related prognostic signature and elucidate its interaction with the immune microenvironment. - Source: PubMed
Publication date: 2026/02/10
Liu HaobinWu YuxiaoSun HaoyuHan XiaoLiu QianZhang YueningZhang Jinling - Accurate preoperative evaluation of lymph node metastasis (LNM) status in patients with papillary thyroid carcinoma (PTC) is essential for the development of individualized diagnosis and treatment strategies; however, the predictive performance of current clinical approaches remains limited. This study aims to identify key molecular biomarkers associated with LNM in PTC, construct LNM-risk prediction models using machine learning (ML) algorithms, and assess their potential value in supporting clinical decision-making. - Source: PubMed
Zhan ZhijunChen LuSun YanZeng JiaxingLi NingYin JundaTan HailongChang Shi - : Triple-negative breast cancer (TNBC), defined by the absence of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER-2) expression, is associated with increased mutation rates. Extracellular vesicles (EVs) play a pivotal role in TNBC progression. This study aimed to analyze mutations and identify EV-related biomarkers for TNBC by employing TNBC-related datasets and EV-related genes (EVRGs). : Initially, mutations in TNBC patients were examined. Differentially expressed EVRGs (DE-EVRGs) were identified by integrating the results of both differential expression analysis and weighted gene co-expression network analysis (WGCNA). Biomarkers were identified using Receiver Operating Characteristic (ROC) and Kaplan-Meier (K-M) analyses. Finally, functional enrichment, drug prediction, molecular docking, and reverse transcription quantitative polymerase chain reaction (RT-qPCR) analyses were performed. : Waterfall plots indicated that exhibited the highest mutation frequency in both the mutation (MUT) and wild-type (WT) group. Four distinct types of immune cells (for example, eosinophils and neutrophils) showed significantly elevated expression levels in the WT group. Notably, was identified as a biomarker of TNBC and its expression was significantly lower in TNBC ( = 0.0025). Functional analysis demonstrated that is enriched in the "drug metabolism cytochrome P450" pathway. Finally, 20 drugs targeting were identified, among which leukotriene C4 demonstrated a binding affinity of -7.2 kcal/mol. This finding suggests that leukotriene C4 has potential therapeutic applications for the treatment of TNBC. : Our study found significant differences between the MUT and WT groups, identifying as a biomarker for TNBC and offering a theoretical basis for TNBC treatment. - Source: PubMed
Publication date: 2026/01/14
Hu YuqiuWu JialiSun LuXie ZishanLi MingYuan LuHuang RuiZhang Weixing