Beyond the nervous system<unk>  is a peripheral lipoprotein<unk>  that functions in lipoprotein metabolism, cardiac fatty acid metabolism, and fat deposition. In effect,<unk>  will allow cholesterol to reach tissues from the bloodstream, where it may be used in cellular membranes. In addition, it will allow fatty acids to get into cells where they may be used as an energy source. Overall,<unk>  primarily modulates the extra-hepatic metabolism of triglyceride-rich lipoproteins. Lipoprotein uptake<unk>  only plays a discrete role in lipid metabolism, but is more significant in stressed situations. Mice with double knockouts in<unk>  and<unk>  have higher serum triglyceride levels than those with only a knockout in the<unk>  gene. In addition,<unk>  knockout mice overexpressing<unk>  have decreased serum triglyceride levels. Although fat deposition is close to normal without<unk> , its role gains importance when<unk>  is deficient. Despite this knowledge on its role in lipoprotein uptake, the complete mechanism of lipid metabolism performed by<unk>  is not fully understood. Endocytosis<unk>  is known to employ endocytosis, although the exact mechanism of this process is unknown for this protein. Endocytosis is mediated through NPxY sequences known to signal for<unk>  internalization through clathrin-coated pits. The presence of this sequence in the cytoplasmic tail of<unk>  makes endocytosis possible. In general, lipoprotein<unk> s undergo a process by which they are endocytosed with their ligand into clathrin-coated pits. From here, they are together transported to early and late endosomes until reaching the lysosome. At this point, hydrolysis occurs and lipoprotein is released into the cytoplasm while the<unk> s are recycled back to the cell surface. It is not yet confirmed if<unk>  follows this exact mechanism, but one closely related to it is likely. In the nervous system The reelin pathway, representing<unk> ’s role in the process. In addition to its role throughout the body,<unk>  has a unique role in the brain. It is a key component of the reelin pathway, which functions in neuronal migration.<unk>  links the reelin protein to an intracellular signaling protein, Dab1, that tells the individual neurons where to go within the anatomy of the brain. Mutations in<unk>  often do not lead to major disorganization as seen in reelin mutations. However, a<unk>  mutation does lead to some disorganization primarily located in the cerebellum, where<unk>  is believed to be most prominent. Neuronal migration<unk>  is expressed on migrating neurons to help guide them to their proper location in the brain. This process is part of the reelin pathway, which is responsible for the inside-out formation of the six-layered neocortex. Despite the discovery of this pathway, many of the specifics and molecular mechanisms of this process are still being debated. The presence of two reelin<unk> s,<unk>  and ApoER2, has made it difficult to distinguish each protein’s specific function. Organization of the six layered neocortex. In the absence of<unk> , the neuroblasts of the cortical plate invade the marginal zone above.<unk>  is primarily responsible for the correct layering of pyramidal cells into layer 1 of the cerebral cortex. In particular, the absence of<unk>  may lead to ectopic accumulation of pyramidal cells in this region.<unk>  does not affect the migration of early born cells into an organized layer, but since its absence results in the invasion of these neuroblasts into the marginal zone, it is theorized that<unk>  may encode a “stop signal.” This is supported by the fact that<unk>  is primarily expressed in the cortical plate adjacent to reelin-expressing cells, Cajal–Retzius cells, and in the intermediate zone. However, definitive evidence has not yet been found. In general, reelin binds<unk>  and undergoes endocytosis via clathrin-coated vesicles. Meanwhile, an intracellular protein, Dab1, has a PI/PTB domain that interacts with the NPxY sequence found in the cytoplasmic tail of<unk> . As a result, Dab1 is tyrosine phosphorylated and reelin is degraded. Finally, phosphorylated Dab1 activates an intracellular signaling cascade that directs neuroblasts to their proper location through the alteration of the cytoskeleton. Many of the specifics of this pathway are still being investigated. It is not yet known if Dab1 is phosphorylated as a result of the endocytosis of reelin, or if there is another mechanism at play. In addition to the organization of the neocortex,<unk>  also plays a role in neuronal migration of the hippocampus and the Purkinje cells of the cerebellum. Yet, much information on this process is still unknown.
VLDL receptor
Low-density lipoprotein receptor gene family
Heart-type fatty acid binding protein
Lipoprotein lipase
Apolipoprotein
Tumor-associated glycoprotein 72
Lipoprotein-X
Platelet membrane glycoprotein