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Apolipoprotein E is resistant to intracellular degradation in vitro and in vivo. Evidence for retroendocytosis
Apolipoprotein E is resistant to intracellular degradation in vitro and in vivo. Evidence for retroendocytosis
Apolipoprotein C-III deficiency accelerates triglyceride hydrolysis by lipoprotein lipase in wild-type and apoE knockout mice
Apolipoprotein C-III deficiency accelerates triglyceride hydrolysis by lipoprotein lipase in wild-type and apoE knockout mice
ApoAV reduces plasma triglycerides by inhibiting very low density lipoprotein-triglycerides (VLDL-TG) production and stimulating lipoprotein lipase-mediated VLDL-TG hydrolysis
ApoAV reduces plasma triglycerides by inhibiting very low density lipoprotein-triglycerides (VLDL-TG) production and stimulating lipoprotein lipase-mediated VLDL-TG hydrolysis
The VLDL receptor plays a major role in chylomicron metabolism by enhancing LPL-mediated triglyceride hydrolysis
The VLDL receptor plays a major role in chylomicron metabolism by enhancing LPL-mediated triglyceride hydrolysis
Apolipoprotein AV: Low concentration, high impact
Apolipoprotein AV: Low concentration, high impact
Apolipoproteins modulate the inflammatory response to lipopolysaccharide
Apolipoproteins modulate the inflammatory response to lipopolysaccharide
ApoC-III deficiency prevents hyperlipidemia induced by apoE overexpression
ApoC-III deficiency prevents hyperlipidemia induced by apoE overexpression
Triglyceride-rich lipoprotein metabolism in unique VLDL receptor, LDL receptor, and LRP triple-deficient mice
Triglyceride-rich lipoprotein metabolism in unique VLDL receptor, LDL receptor, and LRP triple-deficient mice
CD36 deficiency in mice impairs lipoprotein lipase-mediated triglyceride clearance
CD36 deficiency in mice impairs lipoprotein lipase-mediated triglyceride clearance
Severe hypertriglyceridemia in human APOC1 transgenic mice is caused by apoC-I-induced inhibition of LPL
Severe hypertriglyceridemia in human APOC1 transgenic mice is caused by apoC-I-induced inhibition of LPL
Acute inhibition of hepatic beta-oxidation in APOE*3Leiden mice does not affect hepatic VLDL secretion or insulin sensitivity
Acute inhibition of hepatic beta-oxidation in APOE*3Leiden mice does not affect hepatic VLDL secretion or insulin sensitivity
Cholesteryl ester transfer protein decreases high-density lipoprotein and severely aggravates atherosclerosis in APOE*3-Leiden mice
Cholesteryl ester transfer protein decreases high-density lipoprotein and severely aggravates atherosclerosis in APOE*3-Leiden mice
Apolipoprotein CI stimulates the response to lipopolysaccharide and reduces mortality in gram-negative sepsis.
Apolipoprotein CI stimulates the response to lipopolysaccharide and reduces mortality in gram-negative sepsis.
Ritonavir impairs lipoprotein lipase-mediated lipolysis and decreases uptake of fatty acids in adipose tissue
Ritonavir impairs lipoprotein lipase-mediated lipolysis and decreases uptake of fatty acids in adipose tissue
Dietary sphingolipids lower plasma cholesterol and triacylglycerol and prevent liver steatosis in APOE*3Leiden mice
Dietary sphingolipids lower plasma cholesterol and triacylglycerol and prevent liver steatosis in APOE*3Leiden mice
Cholesteryl ester transfer protein inhibition: Effect on reverse cholesterol transport?
Cholesteryl ester transfer protein inhibition: Effect on reverse cholesterol transport?
Endogenous apoC-I increases hyperlipidemia in apoE-knockout mice by stimulating VLDL production and inhibiting LPL
Endogenous apoC-I increases hyperlipidemia in apoE-knockout mice by stimulating VLDL production and inhibiting LPL
ApoE plasma levels and risk of cardiovascular mortality in old age
ApoE plasma levels and risk of cardiovascular mortality in old age
Plasma apoAV levels are markedly elevated in severe hypertriglyceridemia and positively correlated with the APOA5 S19W polymorphism
Plasma apoAV levels are markedly elevated in severe hypertriglyceridemia and positively correlated with the APOA5 S19W polymorphism
Apolipoprotein CI aggravates atherosclerosis development in ApoE-knockout mice despite mediating cholesterol efflux from macrophages
Apolipoprotein CI aggravates atherosclerosis development in ApoE-knockout mice despite mediating cholesterol efflux from macrophages
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