Recombinant Human Secreted Phospholipase A2-IIA PLA2G2A
- Known as:
- Recombinant Human Secreted Phospholipase A2-IIA PLA2G2A
- Catalog number:
- enz-290
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- Recombinant Human Secreted Phospholipase A2-IIA PLA2G2A
Related genes to: Recombinant Human Secreted Phospholipase A2-IIA PLA2G2A
- Gene:
- PLA2G2A NIH gene
- Name:
- phospholipase A2 group IIA
- Previous symbol:
- PLA2B, PLA2L
- Synonyms:
- -
- Chromosome:
- 1p36.13
- Locus Type:
- gene with protein product
- Date approved:
- 1989-04-24
- Date modifiied:
- 2016-10-05
Related products to: Recombinant Human Secreted Phospholipase A2-IIA PLA2G2A
Related articles to: Recombinant Human Secreted Phospholipase A2-IIA PLA2G2A
- Uncontrolled inflammation plays an important role in the initiation and progression of tumors. The repeated circulation and continuous stimulation of gallbladder epithelium caused by gallstones is an important risk factor for gallbladder cancer. - Source: PubMed
Publication date: 2024/04/23
Yu HenghaiChen PengHu YingLiu FengWei XiaopingHu Mingdao - The P2X7 receptor, a member of the P2X receptor family, plays a crucial role in various physiological processes, particularly pain perception. Its expression across immune, neuronal, and glial cells facilitates the release of pro-inflammatory molecules, thereby influencing pain development and maintenance, as evidenced by its association with pulpitis in rats. Notably, P2X receptors such as P2X3 and P2X7 are pivotal in dental pain pathways, making them promising targets for novel analgesic interventions. Leveraging graph neural networks (GNNs) presents an innovative approach to model graph data, aiding in the identification of drug targets and prediction of their efficacy, complementing advancements in genomics and proteomics for therapeutic development. In this study, 921 drug-gene interactions involving P2X receptors were accessed through https://www.probes-drugs.org/. These interactions underwent meticulous annotation, preprocessing, and subsequent utilization to train and assess GNNs. Furthermore, leveraging Cytoscape, the CytoHubba plugin, and other bioinformatics tools, gene expression networks were constructed to pinpoint hub genes within these interactions. Through analysis, SLC6A3, SLC6A2, FGF1, GRK2, and PLA2G2A were identified as central hub genes within the context of P2X receptor-mediated drug-gene interactions. Despite achieving a 65 percent accuracy rate, the GNN model demonstrated suboptimal predictive power for gene-drug interactions associated with oral pain. Hence, further refinements and enhancements are imperative to unlock its full potential in elucidating and targeting pathways underlying oral pain mechanisms. - Source: PubMed
Publication date: 2024/04/21
Yadalam Pradeep KumarNatarajan Prabhu ManickamMosaddad Seyed AliHeboyan Artak - NLRP6 plays a crucial role in maintaining intestinal homeostasis by regulating the interaction between the intestinal mucosa and the microbiota. However, the impact of NLRP6 deficiency on intestinal damage following hematopoietic stem cell transplantation (HSCT) remains poorly understood. In this study, we established a syngeneic HSCT mouse model using C57BL/6 mice as donors and NLRP6-/- or C57BL/6 mice as recipients. Our findings revealed that NLRP6 deficiency had minimal influence on peripheral blood cell counts and splenic immune cell proportions in transplanted mice. However, it exacerbated pathological changes in the small intestine on day 14 post-transplantation, accompanied by increased proportions of macrophages, dendritic cells, and neutrophils. Furthermore, the NLRP6 deficiency resulted in elevated expression of MPO and CD11b, while reducing the levels mature caspase-1 and mature IL-1β in the intestine. Moreover, the NLRP6 deficiency disturbed the expression of apoptosis-related molecules and decreased the tight junction protein occludin. Notably, recipient mice with NLRP6 deficiency exhibited lower mRNA expression levels of antimicrobial genes, such as Reg3γ and Pla2g2a. The short-term increase in inflammatory cell infiltration caused by NLRP6 deficiency was associated with intestinal damage, increased apoptosis, reduced expression of antimicrobial peptides, and impaired intestinal repair. Taken together, our findings demonstrate that the loss of NLRP6 exacerbates post-transplantation intestinal damage in recipient mice. - Source: PubMed
Publication date: 2024/04/12
Zhu ShengyunZhang XueXu KairenLiang JingWang WeiweiZeng LingyuXu Kailin - The incidence of ulcerative colitis (UC) continues to rise globally, but effective therapeutic targets are still lacking. In recent years, numerous studies have indicated that lipid therapies could offer a novel perspective for UC treatment. Given the absence of prior research utilizing high-throughput data to identify target genes associated with lipid metabolism, we conducted this work. - Source: PubMed
Publication date: 2024/03/14
Ding XuexuanYan FangfangWang WenjianQin JingtongLuo Lianxiang - Phospholipase A2 (PLA2) enzymes are pivotal in various biological processes, such as lipid mediator production, membrane remodeling, bioenergetics, and maintaining the body surface barrier. Notably, these enzymes play a significant role in the development of diverse tumors. - Source: PubMed
Qiu ChenXiang Yu-KaiDa Xuan-BoZhang Hong-LeiKong Xiang-YuHou Nian-ZongZhang ChengTian Fu-ZhouYang Yu-Long