CETP Activity Assay Kit100 assays
- Known as:
- CETP Activity Assay Kit100 tests
- Catalog number:
- K601-100
- Product Quantity:
- 100 assays
- Category:
- Peptides
- Supplier:
- Biovis
- Gene target:
- CETP Activity Assay Kit100 assays
Related genes to: CETP Activity Assay Kit100 assays
- Gene:
- CETP NIH gene
- Name:
- cholesteryl ester transfer protein
- Previous symbol:
- -
- Synonyms:
- BPIFF
- Chromosome:
- 16q13
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-03-17
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OxiSelect™ In Vitro ROS RNS Assay Kit (Green Fluorescence), Trial Size guanine nucleotide binding protein alpha inhibiting activity polypeptide 1 (GNAI1) polyclonal antibody(1-Kit) 14,15-DHET sEH activity ELISA Kit(10-Kit) 14,15-DHETsEH activity ELISA Kit(2-Kit) 14,15-DHET sEH activity ELISA Kit(5-Kit) 14,15-DHET sEH activity ELISA Kit*B12 Assay Agar Using E.coli Mutant Culture (Harrison et al. Medium) USE For microbiological assay of Vitamin B12 using E.coli mutant 113 _ 3 Davis ATCC 11105.*B12 Assay Medium (Using L. leichmanni) USE For microbiological assay of vitamin B 12 using L.leichmannii ATCC 7830.*B12 Culture Agar (E.coli Maintenance Medium ) (E. coli Mutant Culture Agar) USE For propogation cultivation and maintenance of E.coli mutant used in microbiological assay of vitamin B 12.*B12 Inoculum Broth (L.leichmanni) USE For microbiological assay of vitamin B 12 using Lactobacillus leichmannii ATCC 7830.*Dey_Engley Neutralizing Agar (D_E Agar Disinfectant Testing) USE For disinfectant testing,where neutralization of the chemical is important for determining its bactericidal activity. Related articles to: CETP Activity Assay Kit100 assays
- Hyperlipidemia, a key risk factor for cardiovascular disease, is characterized by elevated low-density lipoprotein cholesterol (LDL-C), triglycerides, and reduced high-density lipoprotein cholesterol (HDL-C). Cholesteryl ester transfer protein (CETP) inhibitors, such as anacetrapib, obicetrapib, evacetrapib, dalcetrapib, and torcetrapib, aim to improve lipid profiles by increasing HDL-C and reducing LDL-C, but their comparative efficacy remains unclear. - Source: PubMed
Khalil IbrahimIslam M RafiqulPromi Sunjida AminJoy Arindam DasSayed Md AbuAcharjee DurjoyAl-Shammari Ali SaadAbrar SakibJamil Ta-Seen BinTaseen MalaikaBiswas SubornaMifty Sumaya KhanAl-Badri Sajjad GhanimDebnath AvijitHossain Md ImranAkter Mahmuda - [This corrects the article DOI: 10.1371/journal.pone.0294764.]. - Source: PubMed
Publication date: 2025/09/12
Ølnes Åsa SchawlannTeigen MarianneLaerdahl Jon KLeren Trond PStrøm Thea BismoBjune Katrine - Cardiovascular disease remains a major global health challenge, with dyslipidaemia being a key modifiable risk factor. While low density lipoprotein cholesterol (LDL-C) is the primary target for lipid-lowering therapies, recent evidence highlights the importance of triglycerides, apolipoprotein B (apoB), and lipoprotein(a) [Lp(a)] for residual cardiovascular risk. Current lipid-lowering therapies target key enzymes and proteins involved in cholesterol and lipid metabolism. Statins inhibit HMG-CoA reductase, reducing cholesterol biosynthesis and increasing LDL receptor (LDLR) expression in the liver. Bempedoic acid inhibits ATP citrate lyase, the enzyme upstream of HMG-CoA reductase in the mevalonate pathway, offering an alternative to statins by selectively acting in the liver, minimizing muscle-related side effects. Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors [evolocumab, alirocumab, inclisiran, lerodalcibep, and enlicitide decanoate (MK0616)] prevent LDLR degradation, while ezetimibe limits intestinal cholesterol absorption. Emerging lipid-lowering targets include angiopoietin-like 3 protein (ANGPTL3) and apolipoprotein C-III (apoC-III). Inhibiting ANGPTL3 reduces both triglycerides and LDL-C independently of LDL receptor. Inhibition of apoC-III unleashes lipoprotein lipase (LPL) activity, promoting triglyceride-rich particle catabolism, even in complete LPL deficiency. Cholesteryl ester transfer protein (CETP) inhibition also increases the catabolism of apoB-containing lipoproteins. Ongoing research into strategies to reduce Lp(a), primarily but not exclusively through antisense therapies, aims to demonstrate the cardiovascular benefits of targeting this lipoprotein. In summary, the field of targets for lipid and lipoprotein lowering is constantly evolving and offers new strategies for patients resistant to current therapies or with specific lipid profile abnormalities. - Source: PubMed
Publication date: 2025/09/05
Ballantyne Christie MNorata Giuseppe D - An increasing body of research indicates an association between lipid-lowering medications and sensorineural hearing loss (SNHL), although there is still controversy. Therefore, the aim of this study is to investigate the genetic correlation between different lipid-lowering therapeutic gene targets and SNHL. The genetic association between lipids, lipid-lowering drug target genes, and SNHL was analyzed using a 2-sample Mendelian randomization approach. The exposures included 5 circulating lipid levels (triglycerides, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, apolipoprotein A-I, and apolipoprotein B) and 10 target genes simulating the effects of lipid-lowering drugs (HMGCR, PCSK9, Niemann-Pick C1-like 1 [NPC1L1], LDLR, APOB, CETP, LPL, ANGPTL3, APOC3, and PPARA). Summary data from a large-scale genome-wide association study on SNHL from the Finnish database were used as the outcome. The inverse variance-weighted method was employed as the primary approach, with sensitivity tests conducted to evaluate heterogeneity and pleiotropy in the results. The genetic prediction of lipid levels was not significantly associated with SSNL. However, genetic proxies for lowering low-density lipoprotein cholesterol, specifically variants in NPC1L1 (OR = 1.943 [95% CI 1.116-3.383]; P = .018) and LDL receptor (LDLR) (OR = 1.279 [95% CI 1.107-1.477]; P < .001), were associated with an increased risk of SNHL. Similarly, a genetic proxy for lowering triglycerides, the apoprotein C-III (APOC3) variant (OR = 1.174 [95% CI 1.054-1.307]; P = .003), was associated with an increased risk of SNHL. After Bonferroni correction, the genetic variants for LDLR and APOC3 remained significantly associated with an increased risk of SNHL, while the association with the NPC1L1 lipid-lowering variant was no longer significant. This study suggests that lipid-lowering medications potentially have a causal impact on increasing the risk of SNHL through the LDLR and APOC3 pathways. LDLR and APOC3 show potential as candidate drug targets for the prevention of SNHL. However, the results of the study and the potential mechanism of action require further experimental validation and evaluation. - Source: PubMed
Yang YanHuang Hao-FeiPu Kun-Lin - 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
Dergunov Alexander DNosova Elena VRozhkova Alexandra VBaserova Veronika BPopov Mikhail AVinogradina Margarita ALimborska Svetlana ADergunova Liudmila V