Abstract
Very Low Density Lipoprotein Receptor (VLDLR) and Apolipoprotein E Receptor 2 (ApoER2) are important receptors in the brain for mediating the signaling effects of the extracellular matrix protein Reelin, affecting neuronal function in development and in the adult brain. VLDLR and ApoER2 are members of the low density lipoprotein family, which also mediates the effects of numerous other extracellular ligands, including apolipoprotein E. Although VLDLR and ApoER2 are highly homologous, they differ in a number of ways, including structural differences, expression patterns, alternative splicing, and binding of extracellular and intracellular proteins. This review aims to summarize important aspects of VLDLR and ApoER2 that may account for interesting recent findings that highlight the unique functions of each receptor.
Highlights
Very Low Density Lipoprotein Receptor (VLDLR) and Apolipoprotein E Receptor 2 (ApoER2; known as LRP8) are members of the LDL receptor family, a group associated with cellular cholesterol homeostasis [1]
VLDLR and ApoER2 are primarily recognized for their role in neural development through Reelin signaling, a process that is responsible for proper positioning of newly generated neurons leading to the inside-out formation of the six-layered neocortex [3]
It is unclear what the specific contributions are for each ApoE receptor or ligand; the use of the ligand Reelin has allowed for the identification of at least three specific pathways associated with ApoER2 and VLDLR activation
Summary
Very Low Density Lipoprotein Receptor (VLDLR) and Apolipoprotein E Receptor 2 (ApoER2; known as LRP8) are members of the LDL receptor family, a group associated with cellular cholesterol homeostasis [1]. Reelin interacts extracellularly with VLDLR and ApoER2, promoting Dab phosphorylation intracellularly, and resulting in downstream effects that regulate proper migration of neurons during development [6,34,73]. Indirect activation of signaling involving calcium-mediated signal transduction pathways occurs through modification and subsequent increase in NMDAR conductance, which in turn can activate the extracellular signal-related kinases 1/2 (ERK1/2) [29,82] It is unclear what the specific contributions are for each ApoE receptor or ligand; the use of the ligand Reelin has allowed for the identification of at least three specific pathways associated with ApoER2 and VLDLR activation. ApoER2 knockout mice or mice lacking exon 19 of ApoER2 show no Reelin-dependent changes in NMDARs or increase in LTP induction
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