VLDLR binds PCSK9

Stable Identifier
R-HSA-8855111
Type
Reaction [binding]
Species
Homo sapiens
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Circulating proprotein convertase subtilisin/kexin type 9 (PCSK9) is an important regulator of plasma cholesterol homeostasis by binding to low-density lipid receptor family members and promoting their degradation in lysosomes (Poirier et al. 2008). In mice, it was observed that circulating PCSK9 can regulate VLDLR protein levels in adipose tissue and thereby, fat accumulation. The absence of PCSK9 led to an increase in lipid uptake resulting in adipocyte hypertrophy which was LDLR-independent (Roubtsova et al. 2011). Whether increased fat deposition also occurs in humans lacking functional PCSK9 remains to be elucidated.

Literature References
PubMed ID Title Journal Year
21273557 Circulating proprotein convertase subtilisin/kexin 9 (PCSK9) regulates VLDLR protein and triglyceride accumulation in visceral adipose tissue

Roubtsova, A, Munkonda, MN, Awan, Z, Marcinkiewicz, J, Chamberland, A, Lazure, C, Cianflone, K, Seidah, NG, Prat, A

Arterioscler. Thromb. Vasc. Biol. 2011
18039658 The proprotein convertase PCSK9 induces the degradation of low density lipoprotein receptor (LDLR) and its closest family members VLDLR and ApoER2

Poirier, S, Mayer, G, Benjannet, S, Bergeron, E, Marcinkiewicz, J, Nassoury, N, Mayer, H, Nimpf, J, Prat, A, Seidah, NG

J. Biol. Chem. 2008
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