Nonsense mutations in hERG cause a decrease in mutant mRNA transcripts by nonsense-mediated mRNA decay in human long-QT syndrome.

Background: Long-QT syndrome type 2 (LQT2) is caused by mutations in the human ether-a-go-go-related gene (hERG). More than 30% of the LQT2 mutations result in premature termination codons. Degradation of premature termination codon-containing mRNA transcripts by nonsense-mediated mRNA decay is incr...

Descripción completa

Detalles Bibliográficos
Publicado en:Circulation Vol. 116; no. 1; pp. 17 - 25
Autores principales: Gong Q, Zhang L, Vincent GM, Horne BD, Zhou Z, Gong, Qiuming, Zhang, Li, Vincent, G Michael, Horne, Benjamin D, Zhou, Zhengfeng
Formato: research Journal Article
Publicado: Lippincott Williams & Wilkins 7/3/2007
Acceso en línea:Ver este registro en EBSCOhost
fields @attributes:
  recordID: 1
pdfLink:
plink: https://search.ebscohost.com/login.aspx?direct=true&db=ccm&AN=105994986&site=ehost-live
header:
  @attributes:
    shortDbName: ccm
    uiTerm: 105994986
    longDbName: CINAHL Complete
    uiTag: AN
  controlInfo:
    bkinfo:
    dissinfo:
    jinfo:
      jid:
        00097322
        1FV
      jtl: Circulation
      issn: 00097322
      maglogo: N
    pubinfo:
      dt: 7/3/2007
      vid: 116
      iid: 1
      pid: 433
      pub: Lippincott Williams & Wilkins
      place: Baltimore, Maryland
    artinfo:
      ui:
        105994986
        105994986
        NLM17576861
        2009624433
        NLM17576861
        PMC2376840
        105994986
      ppf: 17
      ppct: 8
      formats:
      tig:
        atl: Nonsense mutations in hERG cause a decrease in mutant mRNA transcripts by nonsense-mediated mRNA decay in human long-QT syndrome.
      aug:
        au:
          Gong Q
          Zhang L
          Vincent GM
          Horne BD
          Zhou Z
          Gong, Qiuming
          Zhang, Li
          Vincent, G Michael
          Horne, Benjamin D
          Zhou, Zhengfeng
        affil: Division of Cardiovascular Medicine, Oregon Health and Science University, 3181 SW Sam Jackson Park Rd, Portland, OR 97239, USA
      sug:
        subj:
          Carrier Proteins
          Long QT Syndrome
          Mutation
          RNA Metabolism
          Adult
          Aged
          Animals
          Cells Metabolism
          Enzyme Inhibitors Pharmacodynamics
          Female
          Genes
          Genetic Techniques
          Kidney
          Lymphocytes Metabolism
          Male
          Middle Age
          Pedigree
          Piperidines Pharmacodynamics
          Proteins Antagonists and Inhibitors
          Proteins Physiology
          Proteins
          Rats
          Viruses
          Adult: 19-44 years
          Aged: 65+ years
          Middle Aged: 45-64 years
          Female
          Male
      ab: Background: Long-QT syndrome type 2 (LQT2) is caused by mutations in the human ether-a-go-go-related gene (hERG). More than 30% of the LQT2 mutations result in premature termination codons. Degradation of premature termination codon-containing mRNA transcripts by nonsense-mediated mRNA decay is increasingly recognized as a mechanism for reducing mRNA levels in a variety of human diseases. However, the role of nonsense-mediated mRNA decay in LQT2 mutations has not been explored.Methods and Results: We examined the expression of hERG mRNA in lymphocytes from patients carrying the R1014X mutation using a technique of allele-specific transcript quantification. The R1014X mutation led to a reduced level of mutant mRNA compared with that of the wild-type allele. The decrease in mutant mRNA also was observed in the LQT2 nonsense mutations W1001X and R1014X using hERG minigenes expressed in HEK293 cells or neonatal rat ventricular myocytes. Treatment with the protein synthesis inhibitor cycloheximide or RNA interference-mediated knockdown of the Upf1 protein resulted in the restoration of mutant mRNA to levels comparable to that of the wild-type minigene, suggesting that hERG nonsense mutations are subject to nonsense-mediated mRNA decay.Conclusions: These results indicate that LQT2 nonsense mutations cause a decrease in mutant mRNA levels by nonsense-mediated mRNA decay rather than production of truncated proteins. Our findings suggest that the degradation of hERG mutant mRNA by nonsense-mediated mRNA decay is an important mechanism in LQT2 patients with nonsense or frameshift mutations.
      pubtype: Academic Journal
      doctype:
        research
        Journal Article
      ougenre: Article
    language: English
    refInfo:
    holdings:
      @attributes:
        islocal: N