Human Apolipoprotein M ELISA , APOM
- Known as:
- Human Apolipoprotein M Enzyme-linked immunosorbent assay test , APOM
- Catalog number:
- E01A0522
- Product Quantity:
- 96 Tests/kit
- Category:
- -
- Supplier:
- BGene
- Gene target:
- Human Apolipoprotein ELISA APOM
Related genes to: Human Apolipoprotein M ELISA , APOM
- Gene:
- APOM NIH gene
- Name:
- apolipoprotein M
- Previous symbol:
- -
- Synonyms:
- ApoM, G3a, NG20
- Chromosome:
- 6p21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2002-08-02
- Date modifiied:
- 2016-10-05
Related products to: Human Apolipoprotein M ELISA , APOM
Related articles to: Human Apolipoprotein M ELISA , APOM
- It has become clear that elevated HDL-C is not a reliable marker of protection against inflammation and cardiovascular disease (CVD). This review summarizes recent advances in understanding how HDL function is affected by its associated proteins, demonstrating that this is a more appropriate lens through which to assess HDL's protective capacity. - Source: PubMed
Publication date: 2026/08/13
Delk Samuel CReddy Srinivasa T - Visceral and hepatic adiposity and associated inflammation are recognized as prominent features of heart failure (HF) with preserved ejection fraction (HFpEF). Apolipoprotein M (ApoM), a liver-derived lipid-binding protein, exerts anti-inflammatory and cardioprotective effects, and its expression decreases during obesity. However, its role in HFpEF remains unclear. - Source: PubMed
Publication date: 2026/08/09
Yang HongMei ShuaiHe YiCai ZiyangLi FanWang HongJiang Jiangang - Multiple sclerosis (MS) is a severe neuroinflammatory disease causing substantial long-term disability. Strong epidemiologic evidence links Epstein-Barr virus (EBV) exposure with MS risk, but genetic evidence for immune target prioritization in EBV-related phenotypes remains limited. - Source: PubMed
Publication date: 2026/08/05
Zhou YixiangHuang XindiShe XiaoHao QinMi ZhikuanYang Yanling - : We aimed to conduct a comprehensive assessment of how transient iatrogenic hypothyroidism, induced for diagnostic purposes during the follow up of patients with differentiated thyroid cancer, impacts both quantitative and qualitative lipid parameters. : Blood samples were collected during continuous levothyroxine (LT4) supplementation and after four weeks of LT4 withdrawal. In addition to thyroid hormone levels and routine lipid parameters, LDL and HDL subfractions were analyzed using polyacrylamide gel electrophoresis (Lipoprint). Furthermore, the activities of HDL-associated human paraoxonase-1 (PON1) paraoxonase and arylesterase were measured spectrophotometrically, while the levels of myeloperoxidase and apolipoprotein M (ApoM) were determined using ELISA. The activity of key regulators in HDL remodeling was measured using activity assay kits. : In this prospective, single-center study, a total of 52 patients were enrolled (mean age 48 ± 15 years; 13 males and 39 females). Compared to values measured during continuous LT4 supplementation, total cholesterol, HDL-C, LDL-C, ApoA1, and ApoB100 levels were significantly elevated during iatrogenic hypothyroidism ( < 0.0001 for all parameters). Differences in lipoprotein subfraction patterns were also observed: in hypothyroidism, the mean LDL particle size decreased ( = 0.0007) and the proportion of HDL subfractions shifted to the larger HDL subfractions ( < 0.0001). The paraoxonase activity and ApoM level tended to be increased ( = 0.030 and = 0.011, respectively). : In short-term overt hypothyroidism, opposing changes were observed: the shift toward smaller, denser LDL subfractions is considered atherogenic, whereas the increased proportion of larger HDL subfractions, the trend for higher paraoxonase activity and apoM levels can be potentially anti-atherogenic. Our findings further characterize the functional alterations of lipoproteins in hypothyroidism. - Source: PubMed
Publication date: 2026/06/28
Katkó MónikaGazdag AnnamáriaSzentpéteri AnitaLőrincz HajnalkaGalgóczi ErikaErdei AnnamáriaBerta EszterBodor MiklósNagy Endre VHarangi Mariann - Heart failure (HF) is a prevalent cardiovascular disease that significantly impairs quality of life in its advanced stages. Despite a variety of current treatment strategies, the disease burden of HF remains significant. Therefore, exploring novel therapeutic targets is urgently needed. This study utilized Mendelian randomization (MR) to evaluate the causal relationships between druggable genes and HF. Colocalization analysis and summary data-based Mendelian randomization (SMR) were conducted to further validate the relationship between them. Finally, 8 potential therapeutic targets for HF were identified, including 4 risk factors (CYP11A1, GALT, KCNH2, and METRN) and 4 protective factors (APOM, CHD4, IL11RA, and LPAR5). The GO enrichment, KEGG enrichment, and protein-protein interaction (PPI) network analysis indicated that these genes were primarily involved in metabolic regulation and cardiac electrophysiological processes. Moreover, potential drugs targeting these targets were identified using drug prediction and molecular docking, including mitotane, Adehl, Benzofurans, 1,3-Di-o-tolylguanidine, 96-69-5, and bromoenol lactone. Furthermore, PCR results also demonstrated that mitotane might be associated with CYP11A1 and KCNH2. Drugs designed based on these potential therapeutic targets may offer higher success rates and improve clinical outcomes. - Source: PubMed
Publication date: 2026/07/10
Zhu HuilingLuo Suxin