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Most frequent LDL catabolism defects. (A) LDL uptake process by LDLR; (B) class 2 LDLR mutants, LDLR retention in the endoplasmic reticulum; (C) Class 3 mutants, no LDL-LDLR binding; (D) class 4 mutants, impaired LDL-LDLR complex internalization; (E) class 5 mutants, recycling defect; (F) defective ApoB-100 derived impaired LDL-LDLR binding; (G) PCSK9 gain of function mutant.
