IDEAS home Printed from https://ideas.repec.org/a/nat/nature/v423y2003i6939d10.1038_nature01646.html
   My bibliography  Save this article

Role of ERas in promoting tumour-like properties in mouse embryonic stem cells

Author

Listed:
  • Kazutoshi Takahashi

    (Nara Institute of Science and Technology)

  • Kaoru Mitsui

    (Nara Institute of Science and Technology)

  • Shinya Yamanaka

    (Nara Institute of Science and Technology)

Abstract

Embryonic stem (ES) cells are pluripotent cells derived from early mammalian embryos1,2. Their immortality and rapid growth make them attractive sources for stem cell therapies3; however, they produce tumours (teratomas) when transplanted, which could preclude their therapeutic usage4. Why ES cells, which lack chromosomal abnormalities, possess tumour-like properties is largely unknown. Here we show that mouse ES cells specifically express a Ras-like gene, which we have named ERas. We show that human HRasp, which is a recognized pseudogene, does not contain reported base substitutions and instead encodes the human orthologue of ERas. This protein contains amino-acid residues identical to those present in active mutants of Ras5 and causes oncogenic transformation in NIH 3T3 cells. ERas interacts with phosphatidylinositol-3-OH kinase6 but not with Raf7,8. ERas-null ES cells maintain pluripotency but show significantly reduced growth and tumorigenicity, which are rescued by expression of ERas complementary DNA or by activated phosphatidylinositol-3-OH kinase. We conclude that the transforming oncogene ERas is important in the tumour-like growth properties of ES cells.

Suggested Citation

  • Kazutoshi Takahashi & Kaoru Mitsui & Shinya Yamanaka, 2003. "Role of ERas in promoting tumour-like properties in mouse embryonic stem cells," Nature, Nature, vol. 423(6939), pages 541-545, May.
    • Handle: RePEc:nat:nature:v:423:y:2003:i:6939:d:10.1038_nature01646
    DOI: 10.1038/nature01646
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/nature01646
    File Function: Abstract
    Download Restriction: Access to the full text of the articles in this series is restricted.
    File URL: https://libkey.io/10.1038/nature01646?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
    ---><---

    As the access to this document is restricted, you may want to search for a different version of it.

    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:nature:v:423:y:2003:i:6939:d:10.1038_nature01646. 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.