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Cited by 251

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Catalytic Activity Is Not Required for Secreted PCSK9 to Reduce Low Density Lipoprotein Receptors in HepG2 Cells

McNutt, Markey C., Lagace, Thomas A., Horton, Jay D.·2007·Journal of Biological Chemistry
DOI 10.1074/jbc.c700095200PMC PMC13276728
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Crossref · 10.1074/jbc.c700095200

Cites

3 of 3 references verified0 citation errors · 0 not checkable

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  • The post-ER mechanism of PCSK9-mediated LDLr disposal requires the proteolytic activity of PCSK9.

    “The post-ER mechanism requires the proteolytic activity of PCSK9, whereas the endosomallysosomal mechanism does not (Park et al, 2004;McNutt et al, 2007).”

    From PCSK9 is required for the disposal of non-acetylated intermediates of the nascent membrane protein BACE1 (2008) · cites this paper as McNutt et al, 2007

    The Discussion (page not provided) describes intracellular LDLR degradation in a post-ER compartment, but says only that the study does not preclude the possibility that this pathway requires PCSK9 catalytic activity. It does not establish that proteolytic activity is required for the post-ER mechanism. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Mutation of one residue of the PCSK9 catalytic triad abolishes its proteolytic activity and its ability to undergo processing to the C-form.

    “Mutation of one of these residues abolishes the proteolytic activity of PCSK9 and its ability to undergo processing to the C-form (Benjannet et al, 2004(Benjannet et al, , 2006;;McNutt et al, 2007).”

    From PCSK9 is required for the disposal of non-acetylated intermediates of the nascent membrane protein BACE1 (2008) · cites this paper as McNutt et al, 2007

  • The proteolytic activity of PCSK9 requires a catalytic triad of Asp186, His226, and Ser386.

    “The proteolytic activity of PCSK9 requires a triad of residues (Asp 186, His 226 and Ser 386), which constitute the 'catalytic triad' of the protease.”

    From PCSK9 is required for the disposal of non-acetylated intermediates of the nascent membrane protein BACE1 (2008) · cites this paper as McNutt et al, 2007

  • The endosomal-lysosomal mechanism of PCSK9-mediated LDLr disposal does not require the proteolytic activity of PCSK9.

    “The post-ER mechanism requires the proteolytic activity of PCSK9, whereas the endosomallysosomal mechanism does not (Park et al, 2004;McNutt et al, 2007).”

    From PCSK9 is required for the disposal of non-acetylated intermediates of the nascent membrane protein BACE1 (2008) · cites this paper as McNutt et al, 2007

  • PCSK9 is highly expressed in the liver and, upon secretion into plasma, binds to and enhances the degradation of LDLR in a nonenzymatic fashion, thereby increasing circulating LDL cholesterol.

    “The proprotein convertase subtilisin/kexin type 9 (PCSK9) is highly expressed in the liver (2) and, upon its secretion into plasma, binds to and enhances the degradation of the LDLR in a nonenzymatic fashion (3, 4, 5, 6), thereby increasing circulating LDLc.”

    From Asialoglycoprotein receptor 1 is a novel PCSK9-independent ligand of liver LDLR cleaved by furin (2021) · cites this paper as [5]

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Citations

Cites

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Research works printed but not linked: 24

  1. Seidah, 2007, J. Mol. Med.
  2. Seidah, 1997, Curr. Opin. Biotechnol., 8, 602, 10.1016/S0958-1669(97)80036-5 · DOI
  3. Seidah, 2003, Proc. Natl. Acad. Sci. U. S. A., 100, 928, 10.1073/pnas.0335507100 · DOI · Paper page
  4. Benjannet, 1993, Biochem. J., 294, 735, 10.1042/bj2940735 · DOI
  5. Molloy, 1994, EMBO J., 13, 18, 10.1002/j.1460-2075.1994.tb06231.x · DOI
  6. Nakayama, 1997, Biochem. J., 327, 625, 10.1042/bj3270625 · DOI
  7. Cheng, 1999, J. Biol. Chem., 274, 22805, 10.1074/jbc.274.32.22805 · DOI
  8. Naureckiene, 2003, Arch. Biochem. Biophys., 420, 55, 10.1016/j.abb.2003.09.011 · DOI
  9. Benjannet, 2004, J. Biol. Chem., 279, 48865, 10.1074/jbc.M409699200 · DOI · Paper page
  10. Baker, 1993, Curr. Opin. Cell Biol., 5, 966, 10.1016/0955-0674(93)90078-5 · DOI
  11. Anderson, 2002, J. Biol. Chem., 277, 12879, 10.1074/jbc.M108740200 · DOI
  12. Seidah, 2006, Biol. Chem., 387, 871, 10.1515/BC.2006.110 · DOI
  13. Lagace, 2006, J. Clin. Investig., 116, 2995, 10.1172/JCI29383 · DOI · Paper page
  14. Cunningham, 2007, Nat. Struct. Mol. Biol., 14, 413, 10.1038/nsmb1235 · DOI · Paper page
  15. Abifadel, 2003, Nat. Genet., 34, 154, 10.1038/ng1161 · DOI · Paper page
  16. Maxwell, 2004, Proc. Natl. Acad. Sci. U. S. A., 101, 7100, 10.1073/pnas.0402133101 · DOI · Paper page
  17. Park, 2004, J. Biol. Chem., 279, 50630, 10.1074/jbc.M410077200 · DOI · Paper page
  18. Rashid, 2005, Proc. Natl. Acad. Sci. U. S. A., 102, 5374, 10.1073/pnas.0501652102 · DOI · Paper page
  19. Cameron, 2006, Hum. Mol. Genet., 15, 1551, 10.1093/hmg/ddl077 · DOI · Paper page
  20. Zhang, 2007, J. Biol. Chem., 282, 18602, 10.1074/jbc.M702027200 · DOI · Paper page
  21. Reeves, 1996, Proc. Natl. Acad. Sci. U. S. A., 93, 11487, 10.1073/pnas.93.21.11487 · DOI
  22. Zhao, 2006, Am. J. Hum. Genet., 79, 514, 10.1086/507488 · DOI
  23. Maxwell, 2005, Proc. Natl. Acad. Sci. U. S. A., 102, 2069, 10.1073/pnas.0409736102 · DOI · Paper page
  24. Nassoury, 2007, Traffic, 8, 718, 10.1111/j.1600-0854.2007.00562.x · DOI · Paper page

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Metadata

Authors
McNutt, M. C., Lagace, T. A., & Horton, J. D.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2007-07
Volume
282
Issue
29
Pages
20799-20803
ISSN
0021-9258
DOI
10.1074/jbc.c700095200
PMC
PMC13276728
Cited by
251
References
3
Language
en
Licence

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