PLA2G1B
- Known as:
- PLA2G1B
- Catalog number:
- Y213779
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- PLA2G1B
Related genes to: PLA2G1B
- Gene:
- PLA2G1B NIH gene
- Name:
- phospholipase A2 group IB
- Previous symbol:
- PLA2, PPLA2, PLA2A
- Synonyms:
- -
- Chromosome:
- 12q24.31
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2015-11-18
Related products to: PLA2G1B
Related articles to: PLA2G1B
- 4'-Demethyl-epipodophyllotoxin (4'-DMEP) is a precursor of etoposide and has attracted much attention due to its significant antitumor activity. In order to elucidate the molecular mechanism of its inhibition of lung adenocarcinoma (LUAD), this study comprehensively used network pharmacology, machine learning, and molecular simulation technology, and verified it through cell experiments. A total of 171 drug targets and 11,439 disease targets were collected from the public database, and 131 intersection targets were obtained using the Venny tool. Then the 131 targets were visualized by PPI network. Subsequently, 38 significantly differentially expressed targets were screened and identified in the GEPIA database, from which 18 survival-related genes were further screened. GO functions related to mitotic cell cycle regulation and ERK1/ERK2 signaling, as well as KEGG pathways including gap junction and infection-related pathways, were also enriched. Four machine learning models screened five characteristic genes (SLC2A1, TOP2A, MIF, TLR4, and PLA2G1B). Molecular docking confirmed high-affinity interactions (binding energies ≤ -6.1 kcal/mol), a finding that was further validated by molecular dynamics simulation. In vitro experiments revealed that 4'-DMEP inhibited A549 cell proliferation by inducing cell cycle arrest and apoptosis, with significant changes in the expression of SLC2A1, TOP2A, and MIF. These findings not only clarify its molecular mechanism but also provide new ideas for the precise treatment of lung adenocarcinoma. - Source: PubMed
Publication date: 2026/04/03
Yao JinghuiWang ChenhaoWang ZhichaoXiang ShiSun WuChen HuiYang Chao - Cardiovascular diseases (CVDs) still represent a major cause of mortality, with inflammation playing a key role in their pathogenesis. Thus, elucidating the possible effects of disease-modifying antirheumatic drugs (DMARDs) on CVD risk in the general population may hold considerable clinical implications. - Source: PubMed
Publication date: 2026/02/26
Zhuo ChenguiChen LeiSun XiangjieChen TingCai HaipengHu Xiaosheng - The development and progression of bladder cancer are closely linked to its complex tumor microenvironment. and (HD-SB) are commonly used as a prominent herbal pair for treating bladder cancer. However, the pharmacological targets and molecular mechanisms by which HD-SB impacts bladder cancer require further elucidation. Additionally, it remains uncertain whether this herbal pair affects the prognosis and treatment efficacy of bladder cancer. - Source: PubMed
Publication date: 2026/02/13
Liu YuanDuan LiyuanZhu MengweiZhou ZhenzhenZhao PinZhan YonghaoZhang XuepeiZhu Zhaowei - Lung adenocarcinoma (LUAD) in smokers and non-smokers presents distinct clinical characteristics, including differences in genetics, treatment response, and prognosis. To explore these differences, we conducted a meta-analysis using publicly accessible LUAD datasets, identifying meta-differentially expressed genes (DEGs) in smokers and non-smokers. A total of 29meta-DEGs were discovered, with seven (CLDN2, CLDN18, CYP4B1, CYP4X1, FAM83A, HLF, and PLA2G1B) demonstrating prognostic significance in the TCGA-LUAD cohort. Among these, FAM83A was particularly noteworthy for its amplification in LUAD samples and its negative correlation with immune cell infiltration. Functional enrichment analysis revealed key pathways, such as cytochrome P450 metabolism and cell-cell adhesion, which may be critical in LUAD progression. Our findings highlight FAM83A as a potential prognostic biomarker with significant implications for treatment strategies, especially concerning immune modulation. This study offers a more comprehensive insight into the molecular differences in LUAD in smokers and non-smokers and lays the groundwork for targeted therapies tailored to these subgroups. - Source: PubMed
Publication date: 2025/10/08
Singh PrithviRathi AanchalMasood MohammadHassan Md ImtaiyazHaque Mohammad MahfuzulDohare RavinsShamsi Anas - Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by persistent synovial inflammation, progressive cartilage degradation, and osteoclast-mediated bone erosion. While current systemic therapies alleviate inflammation, they often fail to prevent structural joint damage or promote local tissue regeneration. Herein, we developed a chondroitin sulfate methacryloyl (ChSMA) hydrogel-based delivery system encapsulating spermidine (SPD), a naturally occurring polyamine with emerging anti-inflammatory, senescence-attenuating, and chondroprotective properties, to achieve localized and sustained treatment of RA-related joint destruction. Using an RA-mimicking co-culture model comprising RA patient-derived synovial organoids and chondrocytes, we demonstrated that ChSMA@SPD effectively attenuated chondrocyte apoptosis and suppressed the expression of pro-inflammatory cytokines and matrix metalloproteinases (MMPs). In addition, ChSMA@SPD significantly inhibited osteoclast differentiation using primary bone marrow-derived monocytes from mice by downregulating dendritic cell-specific transmembrane protein (DC-STAMP) expression. studies using the collagen-induced arthritis (CIA) mouse model further confirmed that intra-articular administration of ChSMA@SPD reduced arthritis severity, preserved cartilage integrity, and mitigated joint inflammation. Furthermore, network pharmacology and molecular docking analyses identified key signaling pathways and potential molecular targets of SPD, such as TGFB2, XIAP, MMP8, and PLA2G1B. Collectively, our findings highlight ChSMA@SPD as a dual-functional hydrogel platform that simultaneously protects cartilage and suppresses bone resorption, offering a promising localized therapeutic strategy for RA treatment. - Source: PubMed
Publication date: 2025/11/07
Wang XiaochengHe JiaxinHong YixiangJie LigangWu BingShen JinquanZhou GengminWang Qingwen