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PCSK9-mediated degradation of the LDL receptor generates a 17 kDa C-terminal LDL receptor fragment

Tveten, Kristian, Str⊘m, Thea Bismo, Berge, Knut Erik, Leren, Trond P.·2013·Journal of Lipid Research
DOI 10.1194/jlr.m034371
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  • γ-secretase promotes ectodomain shedding of LDLR, decreasing LDLR.

    “γ-secretase Promotes ectodomain shedding of LDLR ↓ [110-112, 114]”

    From The low-density lipoprotein receptor: Emerging post-transcriptional regulatory mechanisms (2025) · cites this paper as [112]

    The Discussion reports that the LDLR fragment was generated during PCSK9-mediated degradation even in the presence of the γ-secretase inhibitor DAPT. The ‘Intracellular degradation of a Class 5 mutant LDLR’ section says ectodomain cleavage precedes γ-secretase cleavage and implicates cysteine cathepsins in generating the fragment. The paper therefore does not present γ-secretase as promoting LDLR ectodomain shedding. (LLM, conf=0.85)

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  • In HepG2 cells, inhibition of γ-secretase with DAPT leads to the appearance of a 17 kDa C-terminal LDLR fragment when exogenous PCSK9 is added.

    “In HepG2 cells inhibition of γ-secretase with DAPT leads to the appearance of a 17 kDa C-terminal LDLR fragment when exogenous PCSK9 is added [112].”

    From The low-density lipoprotein receptor: Emerging post-transcriptional regulatory mechanisms (2025) · cites this paper as [112]

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Research works printed but not linked: 46

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Metadata

Authors
Tveten, K., Str⊘m, T. B., Berge, K. E., & Leren, T. P.
Venue
Journal of Lipid Research
Publisher
Elsevier BV
Published
2013-06
Volume
54
Issue
6
Pages
1560-1566
ISSN
0022-2275
DOI
10.1194/jlr.m034371
Cited by
39
References
0
Language
en
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