LIPG antibody
- Known as:
- LIPG (anti-)
- Catalog number:
- orb100394
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- LIPG antibody
Related genes to: LIPG antibody
- Gene:
- LIPG NIH gene
- Name:
- lipase G, endothelial type
- Previous symbol:
- -
- Synonyms:
- EDL
- Chromosome:
- 18q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-18
- Date modifiied:
- 2016-02-12
Related products to: LIPG antibody
Related articles to: LIPG antibody
- Introducrion : Endothelial lipase gene (LIPG) is implicated in lipid metabolism particularly HDL-C metabolism and in inflammation. Several identified single nucleotide polymorphisms (SNPs) of LIPG were associated with lipoprotein and apolipoprotein metabolism. The implication of LIPG in a chronic inflammation due to multisystemic vasculitis has not been elucidated. - Source: PubMed
Publication date: 2026/03/12
Makhlouf RihabMessedi MeriamSnoussi MounaChaabouni KhansaBen Rhouma BochraBahloul ZouhairMakni Ayadi FatmaJamoussi Kamel - The accuracy of implant positions captured by intraoral scanners (IOSs) is highly dependent on the scanning technique selected. A recently introduced intraoral photogrammetry (PG) system is available; however, its accuracy remains unknown. - Source: PubMed
Publication date: 2026/05/29
Revilla-León MartaCascos RocioBarmak Abdul BKois John CPérez-Barquero Jorge AlonsoGómez-Polo Miguel - Reducing plasma levels of low-density lipoprotein cholesterol (LDL-C) is the cornerstone in the prevention of coronary artery disease (CAD) but may also increase risk of type 2 diabetes (T2D). A comprehensive examination of the genetic evidence of T2D related side-effects of all current lipid-modifying drugs, including those in development, has not yet been performed. - Source: PubMed
Publication date: 2026/05/14
Chen ZekaiTriatin Rima DLuo LiSnieder HaroldSchmidt A FloriaanDitmarsch MarcKastelein John J PDullaart Robin P FKuivenhoven Jan AlbertThio Chris H L - A key methodological challenge for genome-wide association studies is how to leverage haplotype diversity and allelic heterogeneity to improve trait association power, especially in noncoding regions where it is difficult to predict variant impacts and define functional units for variant aggregation. Genealogy-based association methods have the potential to bridge this gap by testing combinations of common and rare haplotypes based purely on their ancestral relationships. In parallel work, we have developed an efficient local ancestry inference engine and a novel statistical method (LOCATER) for combining signals present on different branches of a locus-specific haplotype tree. Here, we develop a genome-wide LOCATER analysis pipeline and apply it to a genome sequencing study of 6795 Finnish individuals with 101 cardiometabolic traits and 18.9 million autosomal variants. We identify 351 significant trait associations at 47 distinct genomic loci and find that LOCATER boosts the single marker test (SMT) association signal at five loci by combining independent signals from distinct alleles. LOCATER successfully recovers known quantitative trait loci not found by SMT, including , recovers known allelic heterogeneity at the gene cluster, and suggests one novel association. We find that confounders have a more pronounced effect on genealogy-based methods than SMT, and we propose a new randomization approach and a general method for genomic control to eliminate their effects. This study demonstrates that genealogy-based methods such as LOCATER excel when multiple causal variants are present and suggests that their application to larger and more diverse cohorts will be fruitful. - Source: PubMed
Publication date: 2026/05/06
Wang XinxinChrist RyanYoung EricaKang Chul JooDas IndranielBelter Edward ALaakso MarkkuAslett Louis J MSteinsaltz DavidStitziel Nathan OHall Ira M - Microplastics are emerging contaminants that pose health risks. They can cause hepatic lipid interventions, but the underlying mechanisms require investigation. This study assessed the retention of polypropylene microplastics in mouse liver and determined the intercorrelations between hepatic lipid fluctuations and transcriptomic changes. Microplastic-induced liver dysfunction was confirmed by the variations of transamination, cholesterol metabolism, biotransformation, and redox state. Chronic high-dose treatment induced distinct pathological changes, including regional fibrotic remodeling and ultrastructural mitochondrial abnormalities. Raman biospectra of liver slice proposed vital peaks of 1060, 1132, 1168, 1340, 1446, 1618, and 1670 cm, representing the liver biomolecule landscapes. Transcriptomic changes were mainly involved in mRNA transcription, multicellular organism development, various stimuli response, cell differentiation, and lipid metabolic process. Microplastic exposure dosage exerted more profound effects than exposure duration on gene expressions of oxidation-reduction process, signal transduction, and lipid metabolism. WGCNA analysis proposed 47 hub genes involved gene expression orchestration, cell fate monitor, and mitochondria translation modulation. Nine differentially expressed genes associated with lipid biomarkers were related to mitochondria transcription ( and ), cell differentiation , and ), lipid catabolism ( and ) and tRNA methyltransferase (), and Raman peak at 1670 cm intimately connected with aggregated forms of protein. Our findings suggested that polypropylene microplastics could change the liver molecular landscape and induce lipid metabolism disorders and transcriptomic changes in mitochondrial protein translation and expression regulation, highlighting their significant consequences in nutrient and energy imbalance. - Source: PubMed
Publication date: 2025/10/29
Wang MiaoWang JingSun XinglinZhang KenaGao JingXu XiaoyingWu JiaruiTao FangfangZhang DayiLiu Mingying