IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v5y2014i1d10.1038_ncomms6410.html
   My bibliography  Save this article

Decreased tumorigenesis in mice with a Kras point mutation at C118

Author

Listed:
  • Lu Huang

    (Duke University Medical Center)

  • John Carney

    (Duke University Medical Center)

  • Diana M. Cardona

    (Duke University Medical Center)

  • Christopher M. Counter

    (Duke University Medical Center
    Duke University Medical Center)

Abstract

KRAS, NRAS or HRAS genes are mutated to encode an active oncogenic protein in a quarter of human cancers. Redox-dependent reactions can also lead to Ras activation in a manner dependent upon the thiol residue of cysteine 118 (C118). Here, to investigate the effect of mutating this residue on tumorigenesis, we introduce a C118S mutation into the endogenous murine Kras allele and expose the resultant mice to the carcinogen urethane, which induces Kras mutation-positive lung tumours. We report that Kras+/C118S and KrasC118S/C118S mice develop fewer lung tumours. Although the KrasC118S allele does not appear to affect tumorigenesis when the remaining Kras allele is conditionally oncogenic, there is a moderate imbalance of oncogenic mutations favouring the native Kras allele in tumours from Kras+/C118S mice treated with urethane. We conclude that the KrasC118S allele impedes urethane-induced lung tumorigenesis.

Suggested Citation

  • Lu Huang & John Carney & Diana M. Cardona & Christopher M. Counter, 2014. "Decreased tumorigenesis in mice with a Kras point mutation at C118," Nature Communications, Nature, vol. 5(1), pages 1-10, December.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms6410
    DOI: 10.1038/ncomms6410
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/ncomms6410
    File Function: Abstract
    Download Restriction: no
    File URL: https://libkey.io/10.1038/ncomms6410?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms6410. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.