Apolipoprotein M (APOM) ELISA Kits

Human Apolipoprotein M (APOM) interaction partners

1. results demonstrated that lower APOM levels in SLE patients and correlated with disease activity.

2. Sequenced the ApoM gene in recurrent venous thromboembolism (VTE) and identified six polymorphisms. ApoM rs805297 was significantly associated with higher risk of VTE recurrence in male but not in female patients.

3. Single nucleotide polymorphism in ApoM gene is associated with chronic obstructive pulmonary disease.

4. ApoM T-855C and T-778C polymorphisms were found to be associated with obesity by regulating HDL (show HSD11B1 ELISA Kits) metabolism, and the T alleles of apoM T-778C were shown to be more strongly correlated.

5. liver mRNA levels of apoM and apoA1 (show APOA1 ELISA Kits) decreased strongly upon sepsis induction.

6. 17beta-estradiol induced up-regulation of apoM in HepG2 cells is through an ER-alpha (show ESR1 ELISA Kits)-dependent pathway involving ER-alpha (show ESR1 ELISA Kits) binding element in the promoter of the apoM gene.

7. A shift in ApoM/sphingosine 1-phosphate between HDL-particles in women with type 1 diabetes mellitus Is associated with impaired anti-inflammatory effects of the ApoM/S1P complex.

8. ApoM-bound sphingosine-1-phosphate regulates adhesion molecule (show NCAM1 ELISA Kits) abundance, leukocyte-endothelial adhesion, and endothelial barrier function via sphingosine-1-phosphate receptor1.

9. HDL (show HSD11B1 ELISA Kits)-associated ApoM is anti-apoptotic by delivering sphingosine 1-phosphate to S1P1 (show S1PR1 ELISA Kits) and S1P3 (show S1PR3 ELISA Kits) receptors on vascular endothelium.

10. Plasma apoM concentrations are higher in patients with hyperlipidaemia than in healthy controls. Low plasma apoM levels in patients with T2DM are likely caused by diabetes but are not induced by hyperlipidaemia.

Mouse (Murine) Apolipoprotein M (APOM) interaction partners

1. This suggests that the autophagy dysfunction caused by the deficiency of ApoM is an important factor in hepatic steatosis (triglyceride accumulation). ApoM plays a key role in normal autophagy activity in the liver and thereby further regulates the metabolism of liver lipids, particularly triglycerides.

2. HDL facilitates S1P efflux from erythrocytes by both apoM-dependent and apoM-independent mechanisms. Moreover, apoM facilitates tubular reabsorption of S1P from the urine, however, with no impact on S1P plasma concentrations.

3. The study suggests that vascular leakage of albumin (show ALB ELISA Kits)-sized particles in ApoM deficiency is S1P (show S1PR1 ELISA Kits)- and S1P1 (show S1PR1 ELISA Kits)-dependent and this dependency exacerbates the response to inflammatory stimuli.

4. apoM might facilitate the maintenance of CD4 (show CD4 ELISA Kits)(+) T-lymphocytes or could modify the T-lymphocytes subgroups in murine spleen

5. Upon immune stimulation, Apom(-/-) mice developed more severe experimental autoimmune encephalomyelitis, characterized by increased lymphocytes in the central nervous system and breakdown of the blood-brain barrier

6. LDL receptor (show LDLR ELISA Kits) and ApoE (show APOE ELISA Kits) have roles in the clearance of ApoM-associated sphingosine 1-phosphate

7. ApoM augmented insulin secretion by maintaining the S1P concentration under both in vivo and in vitro conditions.

8. The present data indicate that the plasma apo-M levels modulate the ability of plasma to mobilize cellular cholesterol, whereas apo-M has no major effect on the excretion of cholesterol into feces.

9. ApoM can bind oxidized phospholipids, increasing the antioxidant effect of HDL (show HSD11B1 ELISA Kits).

10. Results show that apoM, by delivering S1P (show S1PR1 ELISA Kits) to the S1P (show S1PR1 ELISA Kits)(1) receptor on endothelial cells, is a vasculoprotective constituent of HDL (show APOA5 ELISA Kits).