PLTP Activity Assay Kit100 assays
- Known as:
- PLTP Activity Assay Kit100 tests
- Catalog number:
- K604-100
- Product Quantity:
- 100 assays
- Category:
- Peptides
- Supplier:
- Biovis
- Gene target:
- PLTP Activity Assay Kit100 assays
Related genes to: PLTP Activity Assay Kit100 assays
- 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
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- This study investigated the interactive effects of salinity and dietary lipid sources on growth performance, hepatic lipid metabolism, and the underlying molecular mechanisms in spotted sea bass (). Fish were reared at 0‰ or 20‰ salinities and fed diets containing either fish oil (FO) or soybean oil (SO) for 126 days. Results demonstrated that rearing fish at 20‰ salinity significantly enhanced growth performance but concurrently increased hepatic lipid accumulation compared to rearing at 0‰ salinity. Under the same salinity conditions, dietary lipid sources had no significant effect on fish growth performance, however, compared to FO-based diet the SO-based diet significantly increased hepatic lipid accumulation. Salinity significantly enhanced the growth-promoting effect of SO-based diet, but also aggravated hepatic lipid accumulation in fish. The combination of salinity and FO significantly inhibited lipid synthesis (FAS and ACC activities) and lipolysis (ATGL, MGL activities). RNA-seq identified 9,854 common differentially expressed genes (DEGs). GO enrichment analysis revealed that salinity primarily altered processes related to membrane integrity and energy metabolism, whereas lipid sources regulated organelle structure and fatty acid synthesis. Their interaction regulated catalytic activity and membrane integration processes. KEGG pathway analysis identified salinity-driven shifts in energy/carbohydrate metabolism and lipid-energy sensing, whereas lipid sources dominated fatty acid synthesis. GSEA further highlighted lipid source-dependent regulation of glycerolipid metabolism and unsaturated fatty acid synthesis, alongside salinity-responsive pathways including Ppar signaling and steroid biosynthesis. Key lipid-related genes () exhibited differential expression patterns modulated by salinity-lipid interactions. These results support the development of precise nutritional strategies for raising spotted sea bass in varying salinity environments. Replacing FO with SO across salinities is viable when combined with functional additives to regulate lipid metabolism; however, SO inclusion rates should be adjusted downward in seawater to minimize lipid accumulation and optimize performance. - Source: PubMed
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Jin GuoxiongZhang LuAi QinghuiMai KangsenChen Xiaoru - The goal of this study was examination of the association between the expression levels of the genes involved in high-density lipoprotein metabolism and atherogenesis and underlying metabolic pathways and the number of stenotic coronary arteries. Expression of 65 preselected genes in the peripheral blood mononuclear cells of the control patients ( = 63) and patients with coronary artery disease (CAD) with one or two (low stenosis group, = 35) or three or four (high stenosis group, = 41) stenotic vessels, confirmed by coronary angiography, was measured with real-time PCR. Functional enrichment analysis was applied for annotation of differentially expressed genes. Protein products of the differentially expressed genes (DEGs) in the CAD patients compared to the controls were associated with metabolic pathways related to assembly, remodeling, and clearance of plasma lipoproteins, as well as with signaling and regulation of expression of the genes involved in cholesterol transport and efflux. However, comparison of the gene expression profiles and associated metabolic pathways between the groups with high versus low stenosis revealed specific differences between these groups. Expression of the , , , , , , , and genes increased with the increase of the number of stenotic vessels, which suggests involvement of these genes in stenosis expansion via lipoprotein metabolism, inflammation, angiogenesis, and innate immunity. The set of genes , , and was selected as a new gene expression signature of expansion of the coronary artery stenosis, which was validated with the GSE12288 dataset from the Gene Expression Omnibus database, demonstrating an average odds ratio (OR) of 7.49 (95% CI, 2.21 to 25.43). Averaged expression levels of the , , and genes could be used for diagnosis, prognosis evaluation, and treatment of coronary stenosis with strong predictive power. - Source: PubMed
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