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© Michel Huerre
Coupe histologique de foie de patient atteint d'une hépatite C chronique active avec infiltrat (opacité) folliculaire (lymphocytes) (Grossissement X 400). L'hépatite C chronique peut être à l'origine de cirrhose et cancer du foie
Publication : The Journal of biological chemistry

Amyloid Precursor-like Protein 2 and Sortilin Do Not Regulate the PCSK9 Convertase-mediated Low Density Lipoprotein Receptor Degradation but Interact with Each Other

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in The Journal of biological chemistry - 17 Jun 2015

Butkinaree C, Canuel M, Essalmani R, Poirier S, Benjannet S, Asselin MC, Roubtsova A, Hamelin J, Marcinkiewicz J, Chamberland A, Guillemot J, Mayer G, Sisodia SS, Jacob Y, Prat A, Seidah NG

Link to Pubmed [PMID] – 26085104

J. Biol. Chem. 2015 Jul;290(30):18609-20

Capture d’écran 2015-09-03 à 12.31.28Amyloid precursor-like protein 2 (APLP2) and sortilin were reported to individually bind the proprotein convertase subtilisin/kexin type 9 (PCSK9) and regulate its activity on the low-density lipoprotein receptor (LDLR). The data presented herein demonstrate that mRNA knockdowns of APLP2, sortilin, or both in the human hepatocyte cell lines HepG2 and Huh7 do not affect the ability of extracellular PCSK9 to enhance the degradation of the LDLR. Furthermore, mice deficient in APLP2 or sortilin do not exhibit significant changes in liver LDLR or plasma total cholesterol levels. Moreover, cellular overexpression of one or both proteins does not alter PCSK9 secretion, or its activity on the LDLR. We conclude that PCSK9 enhances the degradation of the LDLR independently of either APLP2 or sortilin both ex vivo and in mice. Interestingly, when co-expressed with PCSK9, both APLP2 and sortilin were targeted for lysosomal degradation. Using chemiluminescence proximity and co-immunoprecipitation assays, as well as biosynthetic analysis, we discovered that sortilin binds and stabilizes APLP2, and hence could regulate its intracellular functions on other targets.

http://www.ncbi.nlm.nih.gov/pubmed/26085104