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

A Locked Nucleic Acid Antisense Oligonucleotide (LNA) Silences PCSK9 and Enhances LDLR Expression In Vitro and In Vivo

Gupta, Nidhi, Fisker, Niels, Asselin, Marie-Claude, Lindholm, Marie, Rosenbohm, Christoph, Ørum, Henrik, Elmén, Joacim, Seidah, Nabil G., Straarup, Ellen Marie·2010·PLoS ONE
DOI 10.1371/journal.pone.0010682PMC PMC2871785
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Crossref · 10.1371/journal.pone.0010682

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  • Lack of PCSK9 does not affect the mRNA levels of LDLR, ASGR1, ASGR2, or SREBP2 in HepG2 cells.

    “As expected (18, 19), lack of PCSK9 did not affect the mRNA levels of LDLR. In addition, no effect was observed on the mRNA levels of ASGR1, ASGR2, and the transcription factor SREBP2 implicated in PCSK9 mRNA regulation (20) (Fig. 2C).”

    From Asialoglycoprotein receptor 1 is a novel PCSK9-independent ligand of liver LDLR cleaved by furin (2021) · cites this paper as [19]

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Research works printed but not linked: 33

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  2. M Abifadel, 2003, Mutations in PCSK9 cause autosomal dominant hypercholesterolemia., Nat Genet, 34, 154, 10.1038/ng1161 · DOI · Paper page
  3. KN Maxwell, 2004, Adenoviral-mediated expression of Pcsk9 in mice results in a low-density lipoprotein receptor knockout phenotype., Proc Natl Acad Sci U S A, 101, 7100, 10.1073/pnas.0402133101 · DOI · Paper page
  4. SW 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
  5. S 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
  6. N Nassoury, 2007, The Cellular Trafficking of the Secretory Proprotein Convertase PCSK9 and Its Dependence on the LDLR., Traffic, 8, 718, 10.1111/j.1600-0854.2007.00562.x · DOI · Paper page
  7. DW Zhang, 2008, Structural requirements for PCSK9-mediated degradation of the low-density lipoprotein receptor., Proc Natl Acad Sci U S A, 105, 13045, 10.1073/pnas.0806312105 · DOI · Paper page
  8. HJ Kwon, 2008, Molecular basis for LDL receptor recognition by PCSK9., Proc Natl Acad Sci U S A, 105, 1820, 10.1073/pnas.0712064105 · DOI · Paper page
  9. KN Maxwell, 2005, Overexpression of PCSK9 accelerates the degradation of the LDLR in a post-endoplasmic reticulum compartment., Proc Natl Acad Sci U S A, 102, 2069, 10.1073/pnas.0409736102 · DOI · Paper page
  10. J 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
  11. IK 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
  12. S Rashid, 2005, Decreased plasma cholesterol and hypersensitivity to statins in mice lacking Pcsk9., Proc Natl Acad Sci U S A, 102, 5374, 10.1073/pnas.0501652102 · DOI · Paper page
  13. A Zaid, 2008, Proprotein convertase subtilisin/kexin type 9 (PCSK9): Hepatocyte-specific low-density lipoprotein receptor degradation and critical role in mouse liver regeneration., Hepatology, 48, 646, 10.1002/hep.22354 · DOI · Paper page
  14. Z 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
  15. B Cariou, 2009, PCSK9 dominant negative mutant results in increased LDL catabolic rate and familial hypobetalipoproteinemia., Arterioscler Thromb Vasc Biol, 29, 2191, 10.1161/ATVBAHA.109.194191 · DOI
  16. KM 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
  17. TP 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
  18. RP Naoumova, 2005, Severe hypercholesterolemia in four British families with the D374Y mutation in the PCSK9 gene: long-term follow-up and treatment response., Arterioscler Thromb Vasc Biol, 25, 2654, 10.1161/01.ATV.0000190668.94752.ab · DOI
  19. AJ Hooper, 2007, The C679X mutation in PCSK9 is present and lowers blood cholesterol in a Southern African population., Atherosclerosis, 193, 445, 10.1016/j.atherosclerosis.2006.08.039 · DOI
  20. NG Seidah, 2009, PCSK9 as a therapeutic target of dyslipidemia., Expert Opin Ther Targets, 13, 19, 10.1517/14728220802600715 · DOI · Paper page
  21. G Dubuc, 2009, A new method for measurement of total plasma PCSK9 - clinical application., J Lipid Res, 51, 140, 10.1194/jlr.M900273-JLR200 · DOI
  22. KN Maxwell, 2005, Proprotein convertase subtilisin kexin 9: the third locus implicated in autosomal dominant hypercholesterolemia., Curr Opin Lipidol, 16, 167, 10.1097/01.mol.0000162321.31925.a3 · DOI · Paper page
  23. S Poirier, 2009, Dissection of the endogenous cellular pathways of PCSK9-induced LDLR degradation: Evidence for an intracellular route., J Biol Chem, 284, 28856, 10.1074/jbc.M109.037085 · DOI · Paper page
  24. JC Chan, 2009, A proprotein convertase subtilisin/kexin type 9 neutralizing antibody reduces serum cholesterol in mice and nonhuman primates., Proc Natl Acad Sci U S A, 106, 9820, 10.1073/pnas.0903849106 · DOI · Paper page
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  27. J Elmen, 2008, Antagonism of microRNA-122 in mice by systemically administered LNA-antimiR leads to up-regulation of a large set of predicted target mRNAs in the liver., Nucleic Acids Res, 36, 1153, 10.1093/nar/gkm1113 · DOI
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Metadata

Authors
Gupta, N., Fisker, N., Asselin, M.-C., Lindholm, M., Rosenbohm, C., Ørum, H., Elmén, J., Seidah, N. G., & Straarup, E. M.
Venue
PLoS ONE
Publisher
Public Library of Science (PLoS)
Published
2010-05-17
Volume
5
Issue
5
Pages
e10682
ISSN
1932-6203
DOI
10.1371/journal.pone.0010682
PMC
PMC2871785
Cited by
174
References
3
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (unspecified)

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