This protein aids in the clearance of a molecule whose concentrations are the subject of the "peripheral sink" hypothesis, and a rare isoform of this protein is the major cause of HLP type III.
A domain interaction observed in this protein can be inhibited by the compounds GIND-25 and GIND- 105. That interaction is absent in mice, which lack an Arg-61 residue that interacts with the C-terminal Glu-255 residue of this protein in a human isoform. The major polymorphisms between isoforms of this protein occur on residues 112 and 158, which are occupied by arginine or cysteine. This protein aids in the clearance of a molecule whose concentrations are the subject of the "peripheral sink" hypothesis, and a rare isoform of this protein is the major cause of HLP type III. This protein tightly binds to a protein whose deposits are visualized using PiB. The buildup of NFTs is observed in patients with one isoform of this protein that causes hyperphosphorylation of tau protein. The presence of its 4 variant can lead to the buildup of amyloid plaques, and it normally functions as a lipid transporter. For 10 points, name this protein whose polymorphisms are a leading risk factor for Alzheimer's disease.
A domain interaction observed in this protein can be inhibited by the compounds GIND-25 and GIND- 105.
apolipoprotein E [or APOE; accept apolipoprotein E4 or APOE4 or APOE epsilon 4 or apolipoprotein epsilon 4 or AD2 or LPG or LDLCQ5; prompt on "apolipoprotein" or "APO"]