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Literature summary for 3.4.21.61 extracted from

  • Sun, H.; Samarghandi, A.; Zhang, N.; Yao, Z.; Xiong, M.; Teng, B.B.
    Proprotein convertase subtilisin/kexin type 9 interacts with apolipoprotein B and prevents its intracellular degradation, irrespective of the low-density lipoprotein receptor (2012), Arterioscler. Thromb. Vasc. Biol., 32, 1585-1595.
    View publication on PubMed
Search for more literature for 3.4.21.61

Cloned(Commentary)

Cloned (Comment) Organism
recombinant overexpression of the human enzyme in mouse LDL-receptor null mutant cells, expression and protein profiles, overview. Overexpression of PCSK9 increases plasma ApoB levels in an LDLR-independent fashion Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens Q8NBP7
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Mus musculus Q80W65
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Mus musculus C57BL/6 Q80W65
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Source Tissue

Source Tissue Comment Organism Textmining
heart gene expression but no enzyme protein content Mus musculus
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hepatocyte primary Mus musculus
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kidney gene expression but no enzyme protein content Mus musculus
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liver highest gene expression level, enzyme protein content Mus musculus
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additional information in LDL-receptor null mutant cells, gene expression and protein profiles, overview Mus musculus
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small intestine enzyme protein content Mus musculus
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spleen low gene expression level, gene expression but no enzyme protein content Mus musculus
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Synonyms

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

General Information

General Information Comment Organism
physiological function proprotein convertase subtilisin/kexin type 9 negatively regulates the low-density lipoprotein (LDL) receptor in hepatocytes and plays an important role in controlling circulating levels of LDL-cholesterol. It interacts with apolipoprotein B and prevents its intracellular degradation, irrespective of the low-density lipoprotein receptor, resulting in results in increased secretion of apoB-containing lipo­proteins and increased levels of cholesterol and triacylglycerol. PCSK9/apoB interaction results in increased production of apoB, possibly through the inhibition of intracellular apoB degradation via the autophagosome/lysosome pathway. Role for the enzyme in shuttling between apoB and LDLR-receptor Homo sapiens
physiological function proprotein convertase subtilisin/kexin type 9 negatively regulates the low-density lipoprotein (LDL) receptor in hepatocytes and plays an important role in controlling circulating levels of LDL-cholesterol. It interacts with apolipoprotein B and prevents its intracellular degradation, irrespective of the low-density lipoprotein receptor, resulting in results in increased secretion of apoB-containing lipo­proteins and increased levels of cholesterol and triacylglycerol. PCSK9/apoB interaction results in increased production of apoB, possibly through the inhibition of intracellular apoB degradation via the autophagosome/lysosome pathway. Role for the enzyme in shuttling between apoB and LDLR-receptor Mus musculus