Author: Braun, Elisabeth; Sauter, Daniel
Title: Furin-mediated protein processing in infectious diseases and cancer Document date: 2019_8_5
ID: k3m72uxw_5
Snippet: Although PCSKs are frequently coexpressed in the same cell and may cleave the same substrates, there is no complete redundancy and the inactivation of individual PCSKs results in specific knock-out phenotypes in mice. 6 PCSK1-7 cleave their substrates after basic residues, with the typical recognition motif K/R-X n -K/R↓ 6 ( Table 1 ). In contrast, PCSK8 cleaves after nonbasic residues and is best known for its regulation of cholesterol and lip.....
Document: Although PCSKs are frequently coexpressed in the same cell and may cleave the same substrates, there is no complete redundancy and the inactivation of individual PCSKs results in specific knock-out phenotypes in mice. 6 PCSK1-7 cleave their substrates after basic residues, with the typical recognition motif K/R-X n -K/R↓ 6 ( Table 1 ). In contrast, PCSK8 cleaves after nonbasic residues and is best known for its regulation of cholesterol and lipid metabolism by activating sterol regulatory element-binding protein (SREBP) transcription factors. 6, 7 Like PCSK8, PCSK9 also plays a key role in cholesterol metabolism as it regulates low-density lipoprotein (LDL) particle levels in the blood. However, this effect does not involve proteolytic cleavage of a specific substrate, but is mediated by a direct binding of PCSK9 to LDL receptors. 8 With two FDA-approved inhibitors for the treatment of hypercholesterolaemia, PCSK9 is also the prime example of a protease that is successfully targeted for therapy. 6
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