HIGHLIGHTS
SUMMARY
Kim et_al, showed that LDLR over-expression reduced brain ApoE levels and amyloid β aggregation, while further work from the same laboratory showed that LDLR overexpression in the brain increased the rate of brain-to-blood clearance of both exogenously administered and endogenous Aβ. Chen et_al, have demonstrated that the reduced expression of LDLR in hepatocellular carcinoma cells impairs LDL uptake but promotes proliferation and metastasis in_vitro and in_vivo by activating MEK/ERK. In U87 cells, Song et_al, have proposed that phosphorylated ERK is a potential mediator of LRP1-regulated MMP expression. An additional piece . . .
If you want to have access to all the content you need to log in!
Thanks :)
If you don't have an account, you can create one here.