sPLA2 Activity Kit
- Known as:
- sPLA2 Activity Kit
- Catalog number:
- ASA907-002
- Product Quantity:
- 96 Well
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- sPLA2 Activity Kit
Ask about this productRelated genes to: sPLA2 Activity Kit
- Gene:
- PLA2G2D NIH gene
- Name:
- phospholipase A2 group IID
- Previous symbol:
- -
- Synonyms:
- sPLA2S
- Chromosome:
- 1p36.12
- Locus Type:
- gene with protein product
- Date approved:
- 1999-11-19
- Date modifiied:
- 2015-11-18
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- Oral squamous cell carcinoma (OSCC) is a biologically heterogeneous malignancy with poor clinical outcomes. Hypoxia and lipid metabolic reprogramming are important drivers of OSCC progression and treatment adaptation, and these processes are biologically interconnected. However, prognostic studies integrating hypoxia- and lipid metabolism-related features in OSCC remain limited. Here, transcriptomic data from TCGA-HNSC-OSCC were integrated with curated hypoxia- and lipid metabolism-related genes to identify candidate genes, construct a prognostic signature, and characterize its biological relevance through enrichment analysis, immune profiling, single-cell RNA-sequencing analysis, and RT-qPCR validation. A four-gene signature consisting of STC2, CAV1, ACADL, and PLA2G2D showed stable prognostic performance in the TCGA-HNSC-OSCC cohort and the external validation cohort GSE41613. The risk signature remained significantly associated with overall survival after adjustment for clinicopathological factors and retained prognostic discrimination across stage- and nodal status-defined subgroups. The high- and low-risk groups displayed distinct pathway, immune, mutational, and predicted drug sensitivity features. Notably, PLA2G2D showed the strongest association with differential immune infiltration, whereas single-cell analysis identified endothelial cells as a major CAV1-enriched population with active intercellular communication and dynamic state transitions. These findings define a hypoxia- and lipid metabolism-related prognostic signature and support its relevance to immune remodeling and endothelial cell context in OSCC. - Source: PubMed
Publication date: 2026/05/19
Zhao LiWang JialeJiang KaiyuanWang KunZhang Linglin - Drug-resistant tuberculosis poses a significant global challenge necessitating the prompt advancement of novel therapeutic options. Nonetheless, disease prognosis is contingent upon multiple factors. mRNA and other small RNAs are essential for gene regulation and disease progression. Additionally, they are essential for the advancement of TB mRNA therapies. The review aims to evaluate the functions of mRNA and various small RNAs, including lncRNA, miRNA, circRNA, and ceRNA, as interconnected components within the mRNA-miRNA-circRNA axis in Mycobacterium tuberculosis. In this context, the analysis of various genes expressed during transcription is essential; however, the TB group’s mRNA expression levels of the CXCL10, CXCL9, IL1B, and PLA2G2D genes were substantially higher compared to the control group. In addition, EspC, MetE, and PPE15 increased IgG levels. Besides, the inadequate IgG responses to m-ESAT6 and m-EsxI present a noteworthy research opportunity. Evidence that neutralizing antibodies provide protection against viral infections targeted by mRNA vaccines during the COVID-19 pandemic supports this research. mRNA-based vaccination analogues offer potential therapeutic advantages following BCG administration. Mycobacterium avium and Mycobacterium tuberculosis are efficiently inhibited by the mRNA therapy, namely the repRNA-ID91/ID91 + GLA-SE vaccination, which elicits humoral and cellular immune responses. Therefore, the therapeutic use of mRNA, as demonstrated by numerous studies, suggests its potential as an efficacious therapeutic vaccine subsequent to BCG treatment. Also, investigating the ceRNA network and the relationships among miRNA, circRNA, lncRNA, and mRNA in TB study will improve the management of this infection. - Source: PubMed
Publication date: 2026/03/03
Sundaram KarthikeyanRathinam Sridhar - Lung cancer patients with interstitial pneumonia (IP) have limited treatment options due to the risks associated with therapeutic intervention. The underlying causes of IP in these patients are diverse, and there is currently no detailed molecular pathological classification or an established understanding of the effectiveness of anti-fibrotic medications such as nintedanib. This study aimed to elucidate the mechanism of action of nintedanib by analyzing differential RNA expression between normal and fibrotic lung tissues from lung cancer patients with IP. - Source: PubMed
Publication date: 2026/02/05
Kuroda HiroakiMasago KatsuhiroSeto KatsutoshiHorio YoshitsuguSasaki EiichiFujita ShiroMatsushita Hirokazu - The risk of developing melanoma increases with age. Although immune checkpoint blockade (ICB) therapy has shown considerable success, a significant portion of melanoma patients either fail to respond to ICB or eventually develop resistance. This leads to the urgent need for exploring novel treatments. Phospholipase A2 group IID (PLA2G2D) is an inducible enzyme found in myeloid cells, especially in aging dendritic cells (DCs), that exert an immunosuppressive effect by producing anti- or proinflammatory small lipid molecules, including prostaglandin D2 (PGD2). An aging-related increase of PLA2G2D-PGD2 expression makes this signaling a promising target for treating aging-associated diseases. The overexpression of hematopoietic PGD2 synthase identified in both human and mouse melanoma tissue further highlights the potential of PLA2G2D-PGD2-targeting therapy. In this study, we show that the absence of PLA2G2D or the PGD2 receptor, PTGDR, restricts primary tumor growth and lung metastasis of subcutaneously implanted melanoma, as demonstrated using middle-aged Pla2g2d-/- and Ptgdr-/- mice. These therapeutic benefits are linked to increased tumor infiltration of activated γδ T cells, which can be amplified in B16F10-bearing wild-type mice through the adoptive transfer of Ptgdr-/- DCs. These tumor-restraining effects were also confirmed in DC-specific PTGDR-deficient (zDCcrePtgdrfloxp) mice. Mechanistically, the enhanced production of IL-1β by Ptgdr-/- DCs contributes to the activation and accumulation of γδ T cells in tumor tissue. In summary, our findings highlight the effectiveness of targeting the PLA2G2D-PGD2/PTGDR axis to reprogram aging dendritic cells, thereby inhibiting melanoma progression and presenting a promising therapeutic target, particularly for elderly patients. - Source: PubMed
Liu MingDhakal HimaLi HongMurakami MakotoNarumiya ShuhYan JunYaddanapudi KavithaPerlman StanleyZheng Jian - Cervical cancer, in which cervical squamous cell carcinoma (CSCC) accounts for 60-70% of cases, has a poor prognosis and poses a significant health threat to global patients. Lipid metabolism reprogramming is a key driver of tumor progression and tumor microenvironment (TME) regulation, making it a promising target for improving the efficacy of immunotherapy. This study aimed to construct a lipid metabolism prognostic signature (LMPS) in CSCC and identify key genes involved in tumor progression. - Source: PubMed
Publication date: 2025/10/14
Bai GaigaiChen FanghuaQiu JunjunHua Keqin