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Jae Hyun Byun

Researcher at St. Joseph's Healthcare Hamilton

Publications -  12
Citations -  222

Jae Hyun Byun is an academic researcher from St. Joseph's Healthcare Hamilton. The author has contributed to research in topics: Medicine & Endoplasmic reticulum. The author has an hindex of 5, co-authored 5 publications receiving 79 citations. Previous affiliations of Jae Hyun Byun include McMaster-Carr.

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Journal ArticleDOI

Pcsk9 knockout exacerbates diet-induced non-alcoholic steatohepatitis, fibrosis and liver injury in mice

TL;DR: It is demonstrated that PCSK9 can protect against cytotoxicity in cultured liver cells treated with a saturated fatty acid and it is shown that Pcsk9 knockout mice develop increased liver injury in response to a high-fat diet.
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Caffeine blocks SREBP2-induced hepatic PCSK9 expression to enhance LDLR-mediated cholesterol clearance

TL;DR: In this article , the effect of CF on the expression of two bona fide regulators of circulating low-density lipoprotein cholesterol (LDLc) levels; the proprotein convertase subtilisin/kexin type 9 (PCSK9) and the low density Lipoprotein receptor (LDLR) was investigated.
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Caffeine blocks SREBP2-induced hepatic PCSK9 expression to enhance LDLR-mediated cholesterol clearance

TL;DR: In this article , the effect of CF on the expression of two bona fide regulators of circulating low-density lipoprotein cholesterol (LDLc) levels; the proprotein convertase subtilisin/kexin type 9 (PCSK9) and the low density Lipoprotein receptor (LDLR) was investigated.
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Anti-GRP78 autoantibodies induce endothelial cell activation and accelerate the development of atherosclerotic lesions

TL;DR: It is shown that atherosclerotic-prone ApoE-/- mice develop circulating anti- GRP78 autoantibodies that bind to csGRP78 on lesion-resident endothelial cells, and disruption of the interaction between anti-GRP 78 autoant ibodies and csGRp78 represents a therapeutic strategy.
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Loss-of-function PCSK9 mutants evade the unfolded protein response sensor, GRP78, and fail to induce endoplasmic reticulum stress when retained

TL;DR: Given that overexpression of these LOF PCSK9 variants does not cause UPR activation under normal homeostatic conditions, therapeutic strategies aimed at blocking the autocatalytic cleavage of PC SK9 in the ER represent a viable strategy for reducing circulating PCSK 9.