S-nitrosylation of ARH is required for LDL uptake by the LDL receptor
Copyright policy )S-nitrosylation of ARH is required for LDL uptake by the LDL receptor
The LDL receptor (LDLR) relies upon endocytic adaptor proteins for internalization of lipoproteins. The results of this study show that the LDLR adaptor autosomal recessive hypercholesterolemia protein (ARH) requires nitric oxide to support LDL uptake. Nitric oxide nitrosylates ARH at C199 and C286, and these posttranslational modifications are necessary for association of ARH with the adaptor protein 2 (AP-2) component of clathrin-coated pits. In the absence of nitrosylation, ARH is unable to target LDL-LDLR complexes to coated pits, resulting in poor LDL uptake. The role of nitric oxide on LDLR function is specific for ARH because inhibition of nitric oxide synthase activity impairs ARH-supported LDL uptake but has no effect on other LDLR-dependent lipoprotein uptake processes, including VLDL remnant uptake and dab2-supported LDL uptake. These findings suggest that cells that depend upon ARH for LDL uptake can control which lipoproteins are internalized by their LDLRs through changes in nitric oxide.
- The University of Texas Southwestern Medical Center United States
Mice, Knockout, QD415-436, Lipoproteins, VLDL, low density lipoprotein receptor, Nitric Oxide, Biochemistry, Lipoproteins, LDL, Mice, HEK293 Cells, Membrane Microdomains, Receptors, LDL, nitric oxide, autosomal recessive hypercholesterolemia protein, Animals, Humans, Adaptor Proteins, Signal Transducing
Mice, Knockout, QD415-436, Lipoproteins, VLDL, low density lipoprotein receptor, Nitric Oxide, Biochemistry, Lipoproteins, LDL, Mice, HEK293 Cells, Membrane Microdomains, Receptors, LDL, nitric oxide, autosomal recessive hypercholesterolemia protein, Animals, Humans, Adaptor Proteins, Signal Transducing
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