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Literature summary for 3.4.21.61 extracted from

  • Le May, C.; Kourimate, S.; Langhi, C.; Chetiveaux, M.; Jarry, A.; Comera, C.; Collet, X.; Kuipers, F.; Krempf, M.; Cariou, B.; Costet, P.
    Proprotein convertase subtilisin kexin type 9 null mice are protected from postprandial triglyceridemia (2009), Arterioscler. Thromb. Vasc. Biol., 29, 684-690.
    View publication on PubMed
Search for more literature for 3.4.21.61

Localization

Localization Comment Organism GeneOntology No. Textmining
cytoplasm epithelial cells, accumulates at the apical and basolateral sides of the cells Homo sapiens 5737
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Organism

Organism UniProt Comment Textmining
Homo sapiens Q8NBP7
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Mus musculus
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Source Tissue

Source Tissue Comment Organism Textmining
Caco-2 cell
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 Homo sapiens
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colon
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 Mus musculus
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enterocyte
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 Homo sapiens
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liver
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 Mus musculus
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small intestine
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 Mus musculus
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small intestine
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 Homo sapiens
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Synonyms

Synonyms Comment Organism
PCSK9
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 Mus musculus
PCSK9
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 Homo sapiens
proprotein convertase subtilisin kexin type 9
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 Mus musculus
proprotein convertase subtilisin kexin type 9
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 Homo sapiens

Expression

Organism Comment Expression
Homo sapiens PCSK9 is expressed throughout the entire small intestine and in enterocytes. PCSK9 is expressed almost exclusively in the epithelial barrier of the duodenum and ileum, both in enterocytes and goblet cells. PCSK9 is 160% upregulated by 0.01 mM pravastatin in CaCo-2 cells after exposure for 48 h up
Mus musculus PCSK9 is expressed throughout the small intestine and colon, at a level which does not vary significantly along the intestinal cephalo-caudal axis, and which is similar to that in the liver up

General Information

General Information Comment Organism
malfunction in addition to its effect on LDL-cholesterol, PCSK9 deficiency may protect against cardiovascular disease by reducing postprandial triglyceridemia: PCSK9-deficient mice show a dramatically decreased postprandial triglyceridemia compared with their wild-type littermates. Intestinal triglyceride output is not quantitatively modified by PCSK9 deletion. PCSK9-/- mice present with a significant reduction of lymphatic apoB secretion compared to PCSK9+/+ mice. PCSK9-/- mice secrete larger triglyceride-rich lipoprotein than wild-type littermates. PCSK9-deficient mice have an increased ability to clear chylomicrons compared to wild-type littermates. The dramatic reduction of postprandial lipemia in PCSK9-/- mice results from the combination of various effects, including the intestinal secretion of larger chylomicrons, and their higher hepatic clearance rate Mus musculus