Journal article
Loss‐of‐function PCSK9 mutants evade the unfolded protein response sensor, GRP78, and fail to induce endoplasmic reticulum stress when retained
Abstract
The proprotein convertase subtilisin/kexin type‐9 (PCSK9) plays a central role in cardiovascular disease (CVD) by degrading hepatic low‐density lipoprotein receptor (LDLR). As such, loss‐of‐function (LOF) PCSK9 variants that fail to exit the endoplasmic reticulum (ER) increase hepatic LDLR levels and lower the risk of developing CVD. The retention of misfolded protein in the ER can cause ER stress and activate the unfolded protein response …
Authors
Lebeau P; Platko K; Al‐Hashimi AA; Byun JH; Lhotak S; Holzapfel N; Gyulay G; Igdoura SA; Cool DR; Trigatti B
Journal
The FASEB Journal, Vol. 32, No. S1, pp. 793.7–793.7
Publisher
Wiley
Publication Date
4 2018
DOI
10.1096/fasebj.2018.32.1_supplement.793.7
ISSN
0892-6638