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The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Inhibitors of AKT kinase increase LDL receptor mRNA expression by two different mechanisms

Bjune, Katrine, Wierød, Lene, Naderi, Soheil·2019·PLOS ONE
DOI 10.1371/journal.pone.0218537PMC PMC6583949
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  • The LDLR mRNA exhibits a cell- and tissue-specific half-life, ranging from about 2 hours in human HepG2 cells to about 3 hours in Hepa 1-6 mouse hepatocytes.

    “The LDLR mRNA exhibits a cell-and tissue specific half-life, ranging from ~2 h in human HepG2 cells and ~3 h in Hepa 1-6 mouse hepatocytes, indicating a potential for rapid modulation of LDLR protein production [21,22].”

    From The low-density lipoprotein receptor: Emerging post-transcriptional regulatory mechanisms (2025) · cites this paper as [21]

    The Results section reports an approximately 2-hour LDLR mRNA half-life in HepG2 cells under several AKT-inhibitor treatments. The paper does not report a 3-hour half-life in Hepa 1-6 mouse hepatocytes; its 3-hour result concerns inhibitor-treated HepG2 cells. Page numbers are unavailable in our copy. (LLM, conf=0.88)

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  • Different research groups have identified more than ten different compounds that enhance LDLR mRNA stability and subsequently increase LDLR protein levels, although the mechanisms and specificity are not fully understood.

    “Adding to the complexity of LDLR mRNA regulation, different research groups have identified more than ten different compounds that enhance LDLR mRNA stability and subsequently increase LDLR protein levels, although the mechanism(s) behind these effects and how specific they are is not yet fully understood [19,21,24,32,[35][36][37][38][39][40][41].”

    From The low-density lipoprotein receptor: Emerging post-transcriptional regulatory mechanisms (2025) · cites this paper as [21]

  • AKT2 regulates stability of LDLR mRNA, decreasing LDLR.

    “AKT2 Regulates stability of LDLR mRNA ↓ [21]”

    From The low-density lipoprotein receptor: Emerging post-transcriptional regulatory mechanisms (2025) · cites this paper as [21]

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Research works printed but not linked: 40

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  8. YK Pak, 1996, Activation of LDL receptor gene expression in HepG2 cells by hepatocyte growth factor, J Lipid Res, 37, 985, 10.1016/S0022-2275(20)42009-7 · DOI
  9. GM Wilson, 1998, Stabilization and cytoskeletal-association of LDL receptor mRNA are mediated by distinct domains in its 3’ untranslated region, J Lipid Res, 39, 1025, 10.1016/S0022-2275(20)33870-0 · DOI · Paper page
  10. T Yashiro, 2011, Chenodeoxycholic acid stabilization of LDL receptor mRNA depends on 3’-untranslated region and AU-rich element-binding protein, Biochem Biophys Res Commun, 409, 155, 10.1016/j.bbrc.2011.04.006 · DOI · Paper page
  11. JR Krycer, 2010, The Akt-SREBP nexus: cell signaling meets lipid metabolism, Trends Endocrinol Metab, 21, 268, 10.1016/j.tem.2010.01.001 · DOI
  12. SF Barnett, 2005, Identification and characterization of pleckstrin-homology-domain-dependent and isoenzyme-specific Akt inhibitors, Biochem J, 385, 399, 10.1042/BJ20041140 · DOI
  13. GL Zhou, 2006, Opposing roles for Akt1 and Akt2 in Rac/Pak signaling and cell migration, J Biol Chem, 281, 36443, 10.1074/jbc.M600788200 · DOI
  14. BD Manning, 2007, AKT/PKB signaling: navigating downstream, Cell, 129, 1261, 10.1016/j.cell.2007.06.009 · DOI · Paper page
  15. K Bjune, 2018, MK-2206, an allosteric inhibitor of AKT, stimulates LDLR expression and LDL uptake: A potential hypocholesterolemic agent, Atherosclerosis, 276, 28, 10.1016/j.atherosclerosis.2018.07.009 · DOI
  16. L Holla, 2010, A chimeric LDL receptor containing the cytoplasmic domain of the transferrin receptor is degraded by PCSK9, Mol Genet Metab, 99, 149, 10.1016/j.ymgme.2009.09.012 · DOI
  17. KJ Livak, 2001, Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method, Methods, 25, 402, 10.1006/meth.2001.1262 · DOI · Paper page
  18. J Oh, 2005, Inhibition of low density lipoprotein receptor expression by long-term exposure to phorbol ester via p38 mitogen-activated protein kinase pathway, J Cell Biochem, 96, 786, 10.1002/jcb.20551 · DOI
  19. L Yan, 2009, Abstract #DDT01-1: MK-2206: A potent oral allosteric AKT inhibitor, Cancer Research, 69, DDT01-1
  20. Y Yu, 2015, Targeting AKT1-E17K and the PI3K/AKT Pathway with an Allosteric AKT Inhibitor, ARQ 092, PLoS ONE, 10, e0140479, 10.1371/journal.pone.0140479 · DOI
  21. L Yang, 2004, Akt/protein kinase B signaling inhibitor-2, a selective small molecule inhibitor of Akt signaling with antitumor activity in cancer cells overexpressing Akt, Cancer Res, 64, 4394, 10.1158/0008-5472.CAN-04-0343 · DOI · Paper page
  22. PG Richardson, 2012, Perifosine, an oral, anti-cancer agent and inhibitor of the Akt pathway: mechanistic actions, pharmacodynamics, pharmacokinetics, and clinical activity, Expert Opin Drug Metab Toxicol, 8, 623, 10.1517/17425255.2012.681376 · DOI
  23. KM Grimshaw, 2010, AT7867 is a potent and oral inhibitor of AKT and p70 S6 kinase that induces pharmacodynamic changes and inhibits human tumor xenograft growth, Mol Cancer Ther, 9, 1100, 10.1158/1535-7163.MCT-09-0986 · DOI
  24. TA Yap, 2011, Preclinical pharmacology, antitumor activity, and development of pharmacodynamic markers for the novel, potent AKT inhibitor CCT128930, Mol Cancer Ther, 10, 360, 10.1158/1535-7163.MCT-10-0760 · DOI
  25. S Zhang, 2017, AT7867 Inhibits Human Colorectal Cancer Cells via AKT-Dependent and AKT-Independent Mechanisms, PLoS ONE, 12, e0169585, 10.1371/journal.pone.0169585 · DOI
  26. G Pinton, 2012, Perifosine as a potential novel anti-cancer agent inhibits EGFR/MET-AKT axis in malignant pleural mesothelioma, PLoS ONE, 7, e36856, 10.1371/journal.pone.0036856 · DOI
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Metadata

Authors
Bjune, K., Wierød, L., & Naderi, S.
ORCID
Bjune, Katrine
Venue
PLOS ONE
Publisher
Public Library of Science (PLoS)
Published
2019-06-19
Volume
14
Issue
6
Pages
e0218537
ISSN
1932-6203
DOI
10.1371/journal.pone.0218537
PMC
PMC6583949
Cited by
8
References
1
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
Nasjonalforeningen for folkehelse (2013.ST.054)

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