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The protein encoded by APOM is an apolipoprotein and member of the lipocalin protein family. Additionally we are shipping Apolipoprotein M Antibodies (168) and Apolipoprotein M Proteins (27) and many more products for this protein.
Showing 10 out of 49 products:
Human Apolipoprotein M ELISA Kit for Sandwich ELISA - ABIN417454
Huang, Liu, Jiang, Sun, Zhang, Liu, Xu: Apolipoprotein m (APOM) levels and APOM rs805297 G/T polymorphism are associated with increased risk of rheumatoid arthritis. in Joint, bone, spine : revue du rhumatisme 2014
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Mouse (Murine) Apolipoprotein M ELISA Kit for Sandwich ELISA - ABIN810844
Kurano, Tsukamoto, Hara, Ohkawa, Ikeda, Yatomi: LDL Receptor and ApoE are Involved in the Clearance of ApoM-associated Sphingosine 1-phosphate. in The Journal of biological chemistry 2014
results do not suggest a diagnostic role for ApoM plasma levels in patients with primary VTE. Moreover, the current study suggests that role of ApoM as a risk factor may differ for primary VTE and recurrent VTE in male patients.
These S1P-induced enhancements in growth factors and chemotactic cytokines in retinal pigment epithelium cells were significantly inhibited by ApoM treatment. Additionally, in vivo experiments using a laser-induced choroidal neovascularization (CNV) murine model demonstrated that intravitreal ApoM injection significantly reduced the progression of CNV formation.
The potential of mean force for sphingosine-1-phosphate unbinding from apoM reflected a large binding strength of more than 60 kJ/mol. This high unbinding free energy for sphingosine-1-phosphate underlines the observed specificity of the physiological effects of sphingosine-1-phosphate as it suggests that the spontaneous release of sphingosine-1-phosphate from apoM is unlikely.
results demonstrated that lower APOM levels in SLE patients and correlated with disease activity.
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.
Single nucleotide polymorphism in ApoM gene is associated with chronic obstructive pulmonary disease.
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.
liver mRNA levels of apoM and apoA1 (show APOA1 ELISA Kits) decreased strongly upon sepsis induction.
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.
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.
apoM-S1P-S1PR1 (show S1PR1 ELISA Kits) signaling might underlie the pathogenesis of ALI and apoM could have physiological benefits to alleviate LPS (show TLR4 ELISA Kits)-induced ALI.
These S1P (show S1PR1 ELISA Kits)-induced enhancements in growth factors and chemotactic cytokines in retinal pigment epithelium cells were significantly inhibited by ApoM treatment. Additionally, in vivo experiments using a laser-induced choroidal neovascularization (CNV) murine model demonstrated that intravitreal ApoM injection significantly reduced the progression of CNV formation.
This study highlights the complexity of Apom/S1P (show S1PR1 ELISA Kits) in atherosclerosis and challenges the notion that the Apom/S1P (show S1PR1 ELISA Kits) complex is anti-atherogenic, at least in Apoe (show APOE ELISA Kits)-deficient mice.
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.
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.
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.
apoM might facilitate the maintenance of CD4 (show CD4 ELISA Kits)(+) T-lymphocytes or could modify the T-lymphocytes subgroups in murine spleen
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
LDL receptor (show LDLR ELISA Kits) and ApoE (show APOE ELISA Kits) have roles in the clearance of ApoM-associated sphingosine 1-phosphate
ApoM augmented insulin secretion by maintaining the S1P concentration under both in vivo and in vitro conditions.
The protein encoded by this gene is an apolipoprotein and member of the lipocalin protein family. It is found associated with high density lipoproteins and to a lesser extent with low density lipoproteins and triglyceride-rich lipoproteins. The encoded protein is secreted through the plasma membrane but remains membrane-bound, where it is involved in lipid transport. Alternate splicing results in both coding and non-coding variants of this gene.
, NG20-like protein
, alternative name: G3a, NG20
, protein G3a
, protein Px