IDEAS home Printed from https://ideas.repec.org/a/nat/nature/v457y2009i7231d10.1038_nature07575.html
   My bibliography  Save this article

ABIN-1 is a ubiquitin sensor that restricts cell death and sustains embryonic development

Author

Listed:
  • Shigeru Oshima

    (University of California at San Francisco, 513 Parnassus Avenue, S-1057, San Francisco, California 94143-0451, USA)

  • Emre E. Turer

    (University of California at San Francisco, 513 Parnassus Avenue, S-1057, San Francisco, California 94143-0451, USA)

  • Joseph A. Callahan

    (University of California at San Francisco, 513 Parnassus Avenue, S-1057, San Francisco, California 94143-0451, USA)

  • Sophia Chai

    (University of California at San Francisco, 513 Parnassus Avenue, S-1057, San Francisco, California 94143-0451, USA)

  • Rommel Advincula

    (University of California at San Francisco, 513 Parnassus Avenue, S-1057, San Francisco, California 94143-0451, USA)

  • Julio Barrera

    (University of California at San Francisco, 513 Parnassus Avenue, S-1057, San Francisco, California 94143-0451, USA)

  • Nataliya Shifrin

    (University of California at San Francisco, 513 Parnassus Avenue, S-1057, San Francisco, California 94143-0451, USA)

  • Bettina Lee

    (University of California at San Francisco, 513 Parnassus Avenue, S-1057, San Francisco, California 94143-0451, USA)

  • Benjamin Yen

    (University of California at San Francisco, 513 Parnassus Avenue, S-1057, San Francisco, California 94143-0451, USA)

  • Tammy Woo

    (University of California at San Francisco, 513 Parnassus Avenue, S-1057, San Francisco, California 94143-0451, USA)

  • Barbara A. Malynn

    (University of California at San Francisco, 513 Parnassus Avenue, S-1057, San Francisco, California 94143-0451, USA)

  • Averil Ma

    (University of California at San Francisco, 513 Parnassus Avenue, S-1057, San Francisco, California 94143-0451, USA)

Abstract

Ubiquitin sensors: vital role for ABIN-1 Oshima et al. this week show that ABIN-1 — a protein that interacts with the ubiquitin-editing enzyme A20 and is thought to negatively influence NF-κB signalling — is essential for life; without it, mice die during embryogenesis with fetal liver apoptosis and anaemia. However, this phenomenon appears unrelated to ABIN-1's role in NF-κB signalling. The authors show that ABIN-1 is ubiquitinated and as such binds to and interferes with components of the TNF-induced signalling complex, the so-called DISC. This prevents programmed cell death and allows proper development. This adds to the emerging role for non-degrading ubiquitin modifications in life and death cell-fate decisions.

Suggested Citation

  • Shigeru Oshima & Emre E. Turer & Joseph A. Callahan & Sophia Chai & Rommel Advincula & Julio Barrera & Nataliya Shifrin & Bettina Lee & Benjamin Yen & Tammy Woo & Barbara A. Malynn & Averil Ma, 2009. "ABIN-1 is a ubiquitin sensor that restricts cell death and sustains embryonic development," Nature, Nature, vol. 457(7231), pages 906-909, February.
    • Handle: RePEc:nat:nature:v:457:y:2009:i:7231:d:10.1038_nature07575
    DOI: 10.1038/nature07575
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/nature07575
    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/nature07575?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.

    Citations

    Citations are extracted by the CitEc Project, subscribe to its RSS feed for this item.
    as


    Cited by:

    1. Cyril Pottier & Fahri Küçükali & Matt Baker & Anthony Batzler & Gregory D. Jenkins & Marka Blitterswijk & Cristina T. Vicente & Wouter Coster & Sarah Wynants & Pieter Walle & Owen A. Ross & Melissa E., 2025. "Deciphering distinct genetic risk factors for FTLD-TDP pathological subtypes via whole-genome sequencing," Nature Communications, Nature, vol. 16(1), pages 1-19, December.

    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:457:y:2009:i:7231:d:10.1038_nature07575. 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.