| 11816 |
P08226 |
APOE_MOUSE |
Apolipoprotein E (Apo-E) |
DISRUPTION PHENOTYPE |
APOE knockout mice display severe hypercholesterolemia associated with impaired clearance of dietary fats (PubMed:1423598). Excess cholesterol is more particularly associated with the atherogenic very low and intermediate density lipoproteins in the plasma (PubMed:1423598). These mice are therefore prone to atherosclerosis (PubMed:1423598). Mice lacking both Cx3cr1 and Apoe show decreased atherogenesis (PubMed:12569158). Animals with a double knockout of APOE and CD36, fed a Western diet for 12 weeks, exhibit much lower levels of CXCL1, CXCL2 and CCL5 mRNA expression in the descending aorta and a corresponding decrease in atherosclerotic lesion formation, compared to APOE single knockout mice (PubMed:23812099). Animals with a double knockout of APOE and TLR4 or TLR6 also have less aortic plaque formation than single knockout mice. All 3 double knockout show lower serum concentrations of IL1A, ILB and IL18 (PubMed:20037584). The melanosomes of APOE knockout mice lack the ellipsoidal shape indicative of deficient PMEL amyloidogenesis. {ECO:0000269|PubMed:12569158, ECO:0000269|PubMed:1423598, ECO:0000269|PubMed:20037584, ECO:0000269|PubMed:23812099, ECO:0000269|PubMed:26387950}. |