PLTP Activity Kit (plasma phospholipid transfer protein)
- Known as:
- PLTP Activity Kit (plasma phospholipid transfer protein)
- Catalog number:
- ELI-6279
- Product Quantity:
- 100 Tests
- Category:
- -
- Supplier:
- Nal Von Minden
- Gene target:
- PLTP Activity Kit (plasma phospholipid transfer protein)
Ask about this productRelated genes to: PLTP Activity Kit (plasma phospholipid transfer protein)
- Gene:
- PLTP NIH gene
- Name:
- phospholipid transfer protein
- Previous symbol:
- -
- Synonyms:
- BPIFE
- Chromosome:
- 20q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1994-09-16
- Date modifiied:
- 2014-11-18
Related products to: PLTP Activity Kit (plasma phospholipid transfer protein)
Related articles to: PLTP Activity Kit (plasma phospholipid transfer protein)
- Age-related macular degeneration (AMD) is a leading cause of visual impairment; however, robust drug targets for primary prevention remain elusive. This study aimed to identify candidate genetic loci and putative genetically supported proteins for AMD through integrative genomics and proteomics. - Source: PubMed
Publication date: 2026/08/14
Chen NingLiu YukangChen ZejunXiang YishenYu Honghua - Tumor-associated macrophages (TAMs) are key components of the colorectal cancer (CRC) microenvironment, yet the transcriptional programs associated with M2 states and their prognostic relevance remain incompletely defined. Here, single-cell RNA-seq analysis of CRC identified macrophages that were further classified into M0-like, M1-like, and M2-like states. Pseudotime analysis identified 311 genes associated with M2-like polarization. Cox and LASSO analyses yielded 16 M2-associated prognostic genes (M2Gs), whose robustness was further validated in an independent dataset. PLTP, NPL, and DCTPP1 were enriched in M2 macrophages in CRC tissues. Knockdown of these genes reduced IL-10-induced M2-like polarization, and conditioned media from knockdown macrophages suppressed the malignant phenotypes of HCT116 cells. Finally, a 16-M2G-based risk model stratified prognosis in TCGA and two independent cohorts. Collectively, our study defines an M2-like TAM-associated transcriptional signature with prognostic relevance in CRC and provides functional evidence that selected M2G modulate macrophage polarization and tumor cell phenotypes. - Source: PubMed
Publication date: 2026/06/05
Li MengDong Lingling - Necrotizing enterocolitis (NEC) is a life-threatening gastrointestinal disease of neonates. This study aimed to identify Lipopolysaccharide-binding protein (LBP) as a potential biomarker for the diagnosis of NEC through multi-omics analyses and validation. - Source: PubMed
Publication date: 2026/05/26
Zou PengjianHou LonglongWei PengfeiSong KaiLu JietingZeng JiahaoLiu YingyanZhong XinChen LizhuHuang YaqiOuyang YuNong TaoTian YanLi WeinianLi LinHe QiumingXia HuiminZhong WeiLiu ZipengLan Chaoting - Growing evidence implicates neuroinflammation, gut-derived endotoxemia, and dysregulated lipid metabolism in the pathogenesis of Parkinson's disease (PD). However, the relationships among circulating lipopolysaccharide (LPS), LPS-handling proteins, systemic inflammatory activation, and lipid fractions remain insufficiently characterized. The aim of this study was to compare LPS levels, LPS-related inflammatory mediators, and plasma lipid parameters between PD patients and matched controls, and to explore correlations among these biomarkers. Twenty PD patients and twenty matched controls underwent fasting venous sampling. Circulating LPS, lipopolysaccharide binding protein (LBP), soluble cluster of differentiation 14 (sCD14), high-sensitivity C-reactive protein (hsCRP), and phospholipid transfer protein (PLTP) were quantified via LAL assay and ELISAs. Serum cholesterol, HDL cholesterol (HDL-C), phospholipids (PLs), HDL-PLs and triacylglycerols (TAGs) were assessed using validated biochemical techniques. LPS concentrations did not differ between groups. However, PD patients showed elevated sCD14 and hsCRP levels, reduced LBP, and increased PLTP. Lipid profiling revealed lower total cholesterol and reduced HDL-associated cholesterol and phospholipids in PD, while TAG levels remained unchanged. Correlation analyses indicated coordinated associations between inflammatory markers and lipid fractions, with distinct interaction patterns in PD compared with controls. These findings support a mechanistic interplay among endotoxemia, innate immune activation, and lipid dysregulation in the pathophysiology of PD. - Source: PubMed
Publication date: 2026/04/22
Della Porta MatteoBarichella MichelaPezzoli GianniCazzola Roberta - Accumulating evidence indicates that exogenous toxins can induce lipid metabolic disorders by influencing the gut microbiome. However, the effects of ammonia nitrogen on the gut microbiota and hepatic lipid metabolism of the burbot (lota lota) remain unknown. Therefore, we integrated biochemical measurements, 16S rDNA sequencing, and transcriptomic analysis to evaluate the impact of 96Â h of ammonia nitrogen exposure on oxidative stress, the immune response, lipid metabolism, and gut microbiota in the liver and intestine of lota lota. In this study, lota lota exhibited oxidative damage and immunosuppression following ammonia nitrogen exposure, as evidenced by decreased antioxidant and immune enzyme activities and a concomitant increase in malondialdehyde (MDA) content. Furthermore, ammonia nitrogen exposure altered gut microbial diversity: the abundance of Proteobacteria decreased, whereas that of Bacteroidota and Firmicutes increased. In addition, transcriptomic analysis revealed that the expression of genes related to fatty acid metabolism (fabp, elovl6, pltp) and gut barrier dysfunction (collagen, ecm) was altered. Notably, lipopolysaccharide (LPS) was identified as a key microbial-derived signal triggered by ammonia nitrogen, as demonstrated by ELISA. The translocation of LPS from gut to liver, resulting from compromised intestinal barrier integrity, activated the gut-liver axis and contributed to hepatic lipid metabolic disorders. Overall, the current study elucidates the gut-liver axis-mediated mechanism of ammonia nitrogen toxicity and provides valuable information for understanding the toxic effects of ammonia nitrogen on lota lota and conserving this threatened cold-water species. - Source: PubMed
Publication date: 2026/05/11
Zhai CunhuaLi YutaoHan HaoxiangMa Bo