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Identification of mRNA binding proteins that regulate the stability of LDL receptor mRNA through AU-rich elements

Li, Hai, Chen, Wei, Zhou, Yue, Abidi, Parveen, Sharpe, Orr, Robinson, William H., Kraemer, Fredric B., Liu, Jingwen·2009·Journal of Lipid Research
DOI 10.1194/jlr.m800375-jlr200
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  • Knockdown of hnRNP D, hnRNP I, and KSRP led to an increase of over 50% in LDLR mRNA levels and a concomitant 40% increase in LDLR protein abundance and LDL uptake.

    “Notably, knockdown of the latter led to an increase of over 50 % in LDLR mRNA levels, and a concomitant 40 % increase in LDLR protein abundance and LDL uptake.”

    From The low-density lipoprotein receptor: Emerging post-transcriptional regulatory mechanisms (2025) · cites this paper as [29]

    The Results report that depletion of hnRNP D, hnRNP I, and KSRP increased LDLR mRNA by more than 50% and increased LDLR protein expression. They report LDL uptake increases of 35%, 50%, and 41%, respectively, but do not give a 40% figure for protein abundance. Thus the claimed magnitude is supported approximately for KSRP-related uptake, not for protein abundance. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • Among the identified RBPs, AUH, CPSF1, and GRSF1 act as stabilizing factors, while hnRNP D, hnRNP I, and KSRP are destabilizing factors.

    “Among these, AUH, CPSF1, and GRSF1 were found to act as stabilizing factors, while hnRNP D, hnRNP I, and KSRP are destabilizing factors [29].”

    From The low-density lipoprotein receptor: Emerging post-transcriptional regulatory mechanisms (2025) · cites this paper as [29]

    The Results report that depleting AUH, CPSF1, or GRSF1 reduced LDLR mRNA expression, consistent with a protective role, but the paper does not establish that these three directly stabilize the mRNA. It explicitly identifies hnRNP D, hnRNP I, and KSRP as negative regulators of LDLR mRNA stability (Abstract; Results). (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • AUH, CPSF1, and GRSF1 bind to AREs in the 3′UTR and stabilize LDLR mRNA, increasing LDLR.

    “AUH, CPSF1, GRSF1 Bind to AREs in the 3′UTR and stabilize LDLR mRNA ↑ [29]”

    From The low-density lipoprotein receptor: Emerging post-transcriptional regulatory mechanisms (2025) · cites this paper as [29]

    The Results (page unavailable) report that depleting AUH, CPSF1, or GRSF1 reduced LDLR mRNA levels by 36–44%, supporting a role in maintaining its expression. But the paper does not establish that these three proteins bind the AREs or directly stabilize LDLR mRNA; its ARE-binding experiments identify hnRNP D, hnRNP I, and KSRP instead. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • CSDE1, hnRNPD, hnRNPI, KSRP, ZFP36L1, and ZFP36L2 bind to AREs in the 3′UTR and lead to degradation of LDLR mRNA, decreasing LDLR.

    “CSDE1, hnRNPD, hnRNPI, KSRP, ZFP36L1, ZFP36L2 Bind to AREs in the 3′UTR and lead to degradation of LDLR mRNA ↓ [29-31]”

    From The low-density lipoprotein receptor: Emerging post-transcriptional regulatory mechanisms (2025) · cites this paper as [29]

    The Abstract (page not provided) states that hnRNP D, hnRNP I, and KSRP bind AREs in the LDLR 3′UTR and that silencing them increases LDLR mRNA and protein levels, supporting their role in promoting decay. The passages do not establish the same binding and decay-promoting role for CSDE1, ZFP36L1, or ZFP36L2. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • HuR and ZFP36L1 were considered likely candidates because they have been reported to modulate LDLR mRNA stability in response to agents that activate ERK and their mechanisms have been partially resolved.

    “These two proteins were considered to be likely candidates, because (1) they have been reported to modulate LDLR mRNA stability in response to agents that activate ERK and (2) the mechanisms underlying their regulatory effect on LDLR mRNA stability have been partially resolved [9,13,14,15].”

    From Triciribine Engages ZFP36L1 and HuR to Stabilize LDLR mRNA (2020) · cites this paper as [13]

    The Results (page not supplied) report that ELAVL1 (HuR) depletion diminished berberine’s effect on LDLR mRNA expression, supporting a role for HuR in the response. Our copy does not report a comparable finding for ZFP36L1 or partially resolve the mechanisms of these two proteins. It identifies berberine-related regulation but does not establish the claimed ERK link for both proteins. (LLM, conf=0.82)

    Experimental — accuracy not yet measured

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Citations

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Research works printed but not linked: 43

  1. Brown, 1997, The SREBP pathway: regulation of cholesterol metabolism by proteolysis of the membrane bound transcription factor, Cell., 89, 331, 10.1016/S0092-8674(00)80213-5 · DOI · Paper page
  2. 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
  3. 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
  4. Abifadel, 2003, Mutations in PCSK9 cause autosomal dominant hypercholesterolemia, Nat. Genet., 34, 154, 10.1038/ng1161 · DOI · Paper page
  5. Maxwell, 2003, Novel putative SREBP and LXR target genes identified by microarray analysis in liver of cholesterol-fed mice, J. Lipid Res., 44, 2109, 10.1194/jlr.M300203-JLR200 · DOI · Paper page
  6. Horton, 2003, Combined analysis of oligonucleotide microarray data from transgenic and knockout mice identifies direct SREBP target genes, Proc. Natl. Acad. Sci. USA., 100, 12027, 10.1073/pnas.1534923100 · DOI · Paper page
  7. Horton, 2007, Molecular biology of PCSK9: its role in LDL metabolism, Trends Biochem. Sci., 32, 71, 10.1016/j.tibs.2006.12.008 · DOI · Paper page
  8. Ross, 1995, mRNA stability in mammalian cells, Microbiol. Rev., 59, 423, 10.1128/mr.59.3.423-450.1995 · DOI · Paper page
  9. Yamamoto, 1984, The human LDL receptor: a cystein-rich protein with multiple Alu sequence in its mRNA, Cell., 39, 27, 10.1016/0092-8674(84)90188-0 · DOI · Paper page
  10. 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
  11. Zhang, 2002, AU-rich element-mediated translational control: complexity and multiple activity of trans-activating factors, Biochem. Soc. Trans., 30, 952, 10.1042/bst0300952 · DOI · Paper page
  12. Barreau, 2005, Survey and summary: AU-rich elements and associated factors: are there unifying principles?, Nucleic Acids Res., 33, 7138, 10.1093/nar/gki1012 · DOI · Paper page
  13. Gherzi, 2006, The RNA-binding protein KSRP promotes decay of b-catenin mRNA and is inactivated by PI3K-AKT signaling, PLoS Biol., 5, e5, 10.1371/journal.pbio.0050005 · DOI
  14. Ruggiero, 2007, Identification of a set of KSRP target transcripts upregulated by PI3K-AKT signaling, BMC Mol. Biol., 8, 28, 10.1186/1471-2199-8-28 · DOI
  15. Raineri, 2004, Roles of AUF1 isoforms, HuR, and BRF1 in ARE-dependent mRNA turnover studied by RNA interference, Nucleic Acids Res., 32, 1279, 10.1093/nar/gkh282 · DOI
  16. Pullmann, 2007, Analysis of turnover and translation regulatory RNA-binding protein expression through binding to cognate mRNAs, Mol. Cell. Biol., 27, 6265, 10.1128/MCB.00500-07 · DOI · Paper page
  17. Liao, 2007, Competitive binding of AUF1 and TIAR to MYC mRNA controls its translation, Nat. Struct. Mol. Biol., 14, 511, 10.1038/nsmb1249 · DOI
  18. David, 2007, FRET-detectable interactions between the ARE binding proteins, HuR and p37AUF1, RNA., 13, 1453, 10.1261/rna.501707 · DOI · Paper page
  19. Abidi, 2005, ERK-dependent regulation of hepatic LDL receptor expression by herbal medicine berberine, Arterioscler. Thromb. Vasc. Biol., 25, 2170, 10.1161/01.ATV.0000181761.16341.2b · DOI · Paper page
  20. Abidi, 2006, The medicinal plant goldenseal is a natural LDL-lowering agent with multiple active components and new action mechanisms, J. Lipid Res., 47, 2134, 10.1194/jlr.M600195-JLR200 · DOI · Paper page
  21. Chen, 2008, Analysis of polymorphisms in 3′ untranslated region of LDL receptor gene and their effect on plasma cholesterol levels and drug response, Int. J. Mol. Med., 21, 345
  22. Lehmann, 2006, Metabolic regulation of ApoB mRNA editing is associated with phosphorylation of APOBEC-1 complementation factor, Nucleic Acids Res., 34, 3299, 10.1093/nar/gkl417 · DOI
  23. Kaufmann, 2004, Human Fip1 is a subunit of CPSF that binds to U-rich RNA elements and stimulates poly(A) polymerase, EMBO J., 23, 616, 10.1038/sj.emboj.7600070 · DOI
  24. Hosoda, 2006, Evidence that poly(A) binding protein C1 binds nuclear pre-mRNA poly(A) tails, Mol. Cell. Biol., 26, 3085, 10.1128/MCB.26.8.3085-3097.2006 · DOI
  25. Behm-Ansmant, 2007, A conversed role for cytoplasmic poly(A)-binding protein 1 (PABPC1) in nonsense-mediated mRNA decay, EMBO J., 26, 1591, 10.1038/sj.emboj.7601588 · DOI
  26. Kajita, 1995, The UUAG-specific RNA binding protein, heterogeneous nuclear ribonucleotprotein D0, J. Biol. Chem., 270, 22167, 10.1074/jbc.270.38.22167 · DOI
  27. Kawamura, 2002, Identification of the nucleocytoplasmic shuttling sequence of heterogeneous nuclear ribonucleoprotein D-like protein JKTBP and its interaction with mRNA, J. Biol. Chem., 277, 2732, 10.1074/jbc.M108477200 · DOI
  28. Ostareck-Lederer, 1998, Cytoplasmic regulatory functions of the KH-domain proteins hnRNPs K and E1/E2, Trends Biochem. Sci., 23, 409, 10.1016/S0968-0004(98)01301-2 · DOI
  29. Thiele, 2004, RNA-binding proteins heterogeneous nuclear ribonucleoprotein A1, E1, and K are involved in post-transcriptional control of collagen I and III synthesis, Circ. Res., 95, 1058, 10.1161/01.RES.0000149166.33833.08 · DOI
  30. Kaneko, 2007, The multifunctional protein p54nrb/PSF recruits the exonuclease XRN2 to facilitate pre-mRNA 3′ processing and transcription termination, Genes Dev., 21, 1779, 10.1101/gad.1565207 · DOI
  31. Bollig, 2003, Affinity purification of ARE-binding proteins identifies polyA-binding protein 1 as a potential substrate in MK2-induced mRNA stabilization, Biochem. Biophys. Res. Commun., 301, 665, 10.1016/S0006-291X(03)00015-9 · DOI
  32. Liu, 1997, Novel mechanism of transcriptional activation of hepatic LDL receptor by oncostatin M, J. Lipid Res., 38, 2035, 10.1016/S0022-2275(20)37134-0 · DOI
  33. Liu, 2000, Identification of a novel sterol-independent regulatory element (SIRE) in the human LDL receptor promoter, J. Biol. Chem., 275, 5214, 10.1074/jbc.275.7.5214 · DOI · Paper page
  34. Paradis, 2007, hnRNP I/PTB can antagonize the splicing repressor activity of SRp30c, RNA., 13, 1, 10.1261/rna.403607 · DOI
  35. Wilson, 1997, Modulation of LDL receptor mRNA stability by phorbol esters in human liver cell culture models, J. Lipid Res., 38, 437, 10.1016/S0022-2275(20)37252-7 · DOI · Paper page
  36. Nakahara, 2002, Bile acids enhance low density lipoprotein receptor gene expression via a MAPK cascade-mediated stabilization of mRNA, J. Biol. Chem., 277, 37229, 10.1074/jbc.M206749200 · DOI · Paper page
  37. Sarkar, 2003, Selective degradation of AU-rich mRNAs promoted by the p37 AUF1 protein isoform, Mol. Cell. Biol., 23, 6685, 10.1128/MCB.23.18.6685-6693.2003 · DOI
  38. Wagner, 1998, Structure and genomic organization of the human AUF1 gene: alternative pre-mRNA splicing generates four protein isoforms, Genomics., 48, 195, 10.1006/geno.1997.5142 · DOI
  39. Lu, 2007, Assembly of AUF1 with eIF4G-poly(A) binding protein complex suggests a translation function in AU-rich mRNA decay, RNA., 12, 883, 10.1261/rna.2308106 · DOI
  40. Laroia, 1999, Control of mRNA decay by heat shock-ubiquitin-proteasome pathway, Science., 284, 499, 10.1126/science.284.5413.499 · DOI
  41. Wagner, 2001, Polypyrimidine tract binding protein antagonizes exon definition, Mol. Cell. Biol., 21, 3281, 10.1128/MCB.21.10.3281-3288.2001 · DOI
  42. Söderberg, 2007, Regulation of the murine inducible nitric oxide synthase gene by dexamethasone involves a heterogenous nuclear ribonucleoprotein I (hnRNP I) dependent pathway, Mol. Immunol., 44, 3204, 10.1016/j.molimm.2007.01.029 · DOI
  43. Liu, 2009, Molecular dissection of human oncostatin M-mediated signal transductions through site-directed mutagenesis, Int. J. Mol. Med., 23, 161

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Metadata

Authors
Li, H., Chen, W., Zhou, Y., Abidi, P., Sharpe, O., Robinson, W. H., Kraemer, F. B., & Liu, J.
Venue
Journal of Lipid Research
Publisher
Elsevier BV
Published
2009-05
Volume
50
Issue
5
Pages
820-831
ISSN
0022-2275
DOI
10.1194/jlr.m800375-jlr200
Cited by
85
References
1
Language
en
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