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This study showed that MWM learning was deteriorated and associated with depression-like tendency in SMS2 KO mice.
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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.
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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.
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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.
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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.
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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
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Thus, imaging mass spectrometry can provide visual assessment of the contribution of SMS2 on acyl-chain- and region-specific sphingomyelin metabolism in the kidneys
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characterization of enzymes catalyzing ceramide phosphoethanolamine biosynthesis in mice
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study reveals that all mouse SMS family members (SMSr, SMS1, and SMS2) have CPE synthase activity
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Increasing ceramide levels in the liver can be achieved by SMS2 inhibition to prevent liver steatosis via PPARgamma suppression.
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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.
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SMS2 deficiency decreases atherosclerosis and inhibits inflammation in mice.
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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.
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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
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Ablation of CerS2 causes changes in intrinsic membrane curvature, leading to strong morphological alterations that promote vesicle adhesion, membrane fusion, and tubule formation.
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SMS1 and SMS2 play distinct roles in regulating local sphingomyelin clustering.
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A deficiency of SMS2 can diminish the extent of pulmonary edema and lung injury.
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SMS2 (Sphingomyelin synthase 2) physiologically contributes to de novo Sphingomyelin biosynthesis and plasma membrane Sphingomyelin levels
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Sphingomyelin synthase 2 is one of the determinants for plasma and liver sphingomyelin levels in mice.
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Sphingomyelin synthase (SMS)2 deficiency in the macrophages reduces atherosclerosis in mice.