Sphingomyelin Synthase 2 Proteine (SGMS2)

Human Sphingomyelin Synthase 2 (SGMS2) Interaktionspartner

1. SMS regulates the expression and function of drug transporters P-gp and MRP2.

2. findings suggest that the C-terminal tails of SMSs are involved in homodimer formation, which is required for efficient transport from the ER.

3. PPARdelta activation may be a potential risk of atherosclerosis through enhancing activity of SMS2

4. F-actin polymerization in the region of HIV-1 membrane fusion was more prominent in Sms2-expressing cells than Sms-deficient cells.

5. SMS1 and SMS2 are capable of regulating TGN-mediated protein trafficking and secretion

6. Data indicate that the increased sphingomyelin mass was due to a rapid and highly specific activation of sphingomyelin synthases SMS1 and SMS2.

7. direct morphological evidence for the pro-atherogenic capabilities of sphingomyelin synthase 2

8. Data show that SMS2 acting as a bifunctional enzyme with both SM and CPE synthase activity.

9. Data show that sphingomyelin synthases SMS1 and SMS2 are co-expressed in a variety of cell types and function as the key Golgi- and plasma membrane-associated SM synthases in human cervical carcinoma HeLa cells, respectively.

10. Results indicate that both synthase (SMS)1 and 2 contribute to sphingomyelin (SM) de novo synthesis and control SM levels in the cells and on the cell membrane including plasma membrane.

11. SMS2 is a key factor in control of sphingomyelin and diacylglycerol metabolism within the cell, and thus it influences apoptosis.

12. SMS2 regulates subcellular pools of diacylglycerol-binding proteins in the Golgi apparatus.

13. SMS2 (Sphingomyelin synthase 2) physiologically contributes to de novo Sphingomyelin biosynthesis and plasma membrane Sphingomyelin levels

14. Both SMS1 and SMS2 contain two histidines and one aspartic acid which are conserved within the lipid phosphate phosphatase superfamily. Site-directed mutagenesis of these amino acids abolished SMS activity without altering cellular distribution.

15. These results suggested that posttranslational palmitoylation is important for determination of the subcellular localization of SMS2.

16. Sphingomyelin synthase 2 is one of the determinants for plasma and liver sphingomyelin levels in mice.

Mouse (Murine) Sphingomyelin Synthase 2 (SGMS2) Interaktionspartner

1. This study showed that MWM learning was deteriorated and associated with depression-like tendency in SMS2 KO mice.

2. These results demonstrate that SMS2 deficiency inhibits DSS-induced colitis and subsequent colitis-associated colon cancer via inhibition of colon epithelial cell-mediated inflammation; therefore, inhibition of SMS2 may be a potential therapeutic target for human colitis and colorectal cancer.

3. It was suggested that very long chain SM but not long chain SM were decreased in SMS2-deficient mice liver and plasma. And the exogenously added very long chain SM (d18:1/24:0) could activate macrophages directly, suggesting a novel role of plasma very long chain SM in modulating macrophage activation and resulting inflammation.

4. These findings suggested that the degree of lung injury was reduced during the acute inflammatory reaction when NFkappaB was inhibited, and that the expression of sphingomyelin synthase 2 may affect the induction of the NFkappaB pathway by lipopolysaccharide through CD14.

5. Study provides a mouse model for fetal alcohol spectrum disorder. Due to the accumulation of ceramide in vivo, SMS2 knockout mice allows to investigate how ceramide regulates alcohol-induced neural apoptosis.

6. study provided evidence that genetic inhibition of SMS2 elevated glucose clearance through activation of glucose uptake into insulin-targeted tissues such as skeletal muscle by a mechanism independent of hepatic SMS2

7. Thus, imaging mass spectrometry can provide visual assessment of the contribution of SMS2 on acyl-chain- and region-specific sphingomyelin metabolism in the kidneys

8. characterization of enzymes catalyzing ceramide phosphoethanolamine biosynthesis in mice

9. study reveals that all mouse SMS family members (SMSr, SMS1, and SMS2) have CPE synthase activity

10. Increasing ceramide levels in the liver can be achieved by SMS2 inhibition to prevent liver steatosis via PPARgamma suppression.

11. Data show that LCAT activity was significantly higher in long chain base biosynthesis protein 2 (Sptlc2)+/- and sphingomyelin synthase 2 (Sms2)-/- mice, but markedly lower in ApoE-/- and Ldlr-/- mice.

12. SMS2 deficiency decreases atherosclerosis and inhibits inflammation in mice.

13. Defects in the stria vascularis with reductions in endocochlear potentials together with hair cell dysfunction may account, at least partially, for hearing impairments in SMS1-/- mice.

14. SMS2 over-expression was probably associated with increased expression of aortic inflammatory biomarkers, as well as decreased numbers of CD34/KDR-positive cells, CACs and CFUs in circulation

15. Ablation of CerS2 causes changes in intrinsic membrane curvature, leading to strong morphological alterations that promote vesicle adhesion, membrane fusion, and tubule formation.

16. SMS1 and SMS2 play distinct roles in regulating local sphingomyelin clustering.

17. A deficiency of SMS2 can diminish the extent of pulmonary edema and lung injury.

18. SMS2 (Sphingomyelin synthase 2) physiologically contributes to de novo Sphingomyelin biosynthesis and plasma membrane Sphingomyelin levels

19. Sphingomyelin synthase 2 is one of the determinants for plasma and liver sphingomyelin levels in mice.

20. Sphingomyelin synthase (SMS)2 deficiency in the macrophages reduces atherosclerosis in mice.