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Cited by 194

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

Secreted PCSK9 downregulates low density lipoprotein receptor through receptor-mediated endocytosis

Qian, Yue-Wei, Schmidt, Robert J., Zhang, Youyan, Chu, Shaoyou, Lin, Aimin, Wang, He, Wang, Xiliang, Beyer, Thomas P., Bensch, William R., Li, Weiming, Ehsani, Mariam E., Lu, Deshun, Konrad, Robert J., Eacho, Patrick I., Moller, David E., Karathanasis, Sotirios K., Cao, Guoqing·2007·Journal of Lipid Research
DOI 10.1194/jlr.m700071-jlr200
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Crossref · 10.1194/jlr.m700071-jlr200

Cites

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  • The endosomal-lysosomal mechanism is dependent on ARH adaptor protein-mediated internalization of the PCSK9 (C-form)-LDLr complex into the endocytic pathway.

    “The endosomal-lysosomal mechanism is dependent on autosomal recessive hypercholesterolaemia (ARH) adaptor proteinmediated internalization of the PCSK9 (C-form)-LDLr complex into the endocytic pathway (Park et al, 2004;Qian 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 Qian et al, 2007

    The Results report that reducing ARH or LDLR expression dramatically reduced PCSK9 endocytosis, and the Discussion proposes that their mediated endocytosis delivers PCSK9 and LDLR to endosomal/lysosomal compartments. The paper does not identify the internalized PCSK9–LDLR complex specifically as containing the “C-form” of PCSK9, so that qualifier is not established by our copy. (LLM, conf=0.82)

    Experimental — accuracy not yet measured

  • Overexpression of full-length PCSK9 in the absence of ARH results in degradation of LDLr through an endocytosis-independent mechanism.

    “Overexpression of full-length PCSK9 in the absence of ARH results in degradation of LDLr through an endocytosis-independent mechanism (Park et al, 2004;Qian et al, 2007) that resembles the post-ER mechanism initially described by Maxwell & Breslow (2004) and Maxwell et al (2005).”

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

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Citations

Cites

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Research works printed but not linked: 18

  1. Cannon, 2005, The IDEAL cholesterol: lower is better, J. Am. Med. Assoc., 294, 2492, 10.1001/jama.294.19.2492 · DOI
  2. Wiviott, 2005, Can low-density lipoprotein be too low? The safety and efficacy of achieving very low low-density lipoprotein with intensive statin therapy: a PROVE IT-TIMI 22 substudy, J. Am. Coll. Cardiol., 46, 1411, 10.1016/j.jacc.2005.04.064 · DOI
  3. Brown, 1999, A proteolytic pathway that controls the cholesterol content of membranes, cells, and blood, Proc. Natl. Acad. Sci. USA., 96, 11041, 10.1073/pnas.96.20.11041 · DOI · Paper page
  4. Abifadel, 2003, Mutations in PCSK9 cause autosomal dominant hypercholesterolemia, Nat. Genet., 34, 154, 10.1038/ng1161 · DOI · Paper page
  5. Timms, 2004, A mutation in PCSK9 causing autosomal-dominant hypercholesterolemia in a Utah pedigree, Hum. Genet., 114, 349, 10.1007/s00439-003-1071-9 · DOI
  6. Leren, 2004, Mutations in the PCSK9 gene in Norwegian subjects with autosomal dominant hypercholesterolemia, Clin. Genet., 65, 419, 10.1111/j.0009-9163.2004.0238.x · DOI
  7. Cameron, 2006, Effect of mutations in the PCSK9 gene on the cell surface LDL receptors, Hum. Mol. Genet., 15, 1551, 10.1093/hmg/ddl077 · DOI · Paper page
  8. Kotowski, 2006, A spectrum of PCSK9 alleles contributes to plasma levels of low-density lipoprotein cholesterol, Am. J. Hum. Genet., 78, 410, 10.1086/500615 · DOI · Paper page
  9. Berge, 2006, Missense mutations in the PCSK9 gene are associated with hypocholesterolemia and possibly increased response to statin therapy, Arterioscler. Thromb. Vasc. Biol., 26, 1094, 10.1161/01.ATV.0000204337.81286.1c · DOI · Paper page
  10. Zhao, 2006, Molecular characterization of loss-of-function mutations in PCSK9 and identification of a compound heterozygote, Am. J. Hum. Genet., 79, 514, 10.1086/507488 · DOI
  11. Seidah, 2003, The secretory proprotein convertase neural apoptosis-regulated convertase 1 (NARC-1): liver regeneration and neuronal differentiation, Proc. Natl. Acad. Sci. USA., 100, 928, 10.1073/pnas.0335507100 · DOI · Paper page
  12. Sakai, 1998, Molecular identification of the sterol-regulated luminal protease that cleaves SREBPs and controls lipid composition of animal cells, Mol. Cell., 2, 505, 10.1016/S1097-2765(00)80150-1 · DOI
  13. Maxwell, 2004, Adenoviral-mediated expression of Pcsk9 in mice results in a low-density lipoprotein receptor knockout phenotype, Proc. Natl. Acad. Sci. USA., 101, 7100, 10.1073/pnas.0402133101 · DOI · Paper page
  14. Park, 2004, Post-transcriptional regulation of low density lipoprotein receptor protein by proprotein convertase subtilisin/kexin type 9a in mouse liver, J. Biol. Chem., 279, 50630, 10.1074/jbc.M410077200 · DOI · Paper page
  15. Rashid, 2005, Decreased plasma cholesterol and hypersensitivity to statins in mice lacking Pcsk9, Proc. Natl. Acad. Sci. USA., 102, 5374, 10.1073/pnas.0501652102 · DOI · Paper page
  16. Benjannet, 2004, NARC-1/PCSK9 and its natural mutants: zymogen cleavage and effects on the low density lipoprotein (LDL) receptor and LDL cholesterol, J. Biol. Chem., 279, 48865, 10.1074/jbc.M409699200 · DOI · Paper page
  17. Lagace, 2006, Secreted PCSK9 decreases the number of LDL receptors in hepatocytes and in livers of parabiotic mice, J. Clin. Invest., 116, 2995, 10.1172/JCI29383 · DOI · Paper page
  18. Maxwell, 2005, Overexpression of PCSK9 accelerates the degradation of the LDLR in a post-endoplasmic reticulum compartment, Proc. Natl. Acad. Sci. USA., 102, 2069, 10.1073/pnas.0409736102 · DOI · Paper page

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Metadata

Authors
Qian, Y.-W., Schmidt, R. J., Zhang, Y., Chu, S., Lin, A., Wang, H., Wang, X., Beyer, T. P., Bensch, W. R., Li, W., Ehsani, M. E., Lu, D., Konrad, R. J., Eacho, P. I., Moller, D. E., Karathanasis, S. K., & Cao, G.
Venue
Journal of Lipid Research
Publisher
Elsevier BV
Published
2007-07
Volume
48
Issue
7
Pages
1488-1498
ISSN
0022-2275
DOI
10.1194/jlr.m700071-jlr200
Cited by
194
References
3
Language
en
Licence

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