IDEAS home Printed from https://ideas.repec.org/a/nat/nature/v416y2002i6880d10.1038_416560a.html
   My bibliography  Save this article

p63 and p73 are required for p53-dependent apoptosis in response to DNA damage

Author

Listed:
  • Elsa R. Flores

    (Massachusetts Institute of Technology, Department of Biology and Center for Cancer Research)

  • Kenneth Y. Tsai

    (Massachusetts Institute of Technology, Department of Biology and Center for Cancer Research
    Harvard–Massachusetts Institute of Technology Division of Health Sciences and Technology)

  • Denise Crowley

    (Massachusetts Institute of Technology, Department of Biology and Center for Cancer Research
    Howard Hughes Medical Institute)

  • Shomit Sengupta

    (Massachusetts Institute of Technology, Department of Biology and Center for Cancer Research
    Howard Hughes Medical Institute)

  • Annie Yang

    (Harvard Medical School)

  • Frank McKeon

    (Harvard Medical School)

  • Tyler Jacks

    (Massachusetts Institute of Technology, Department of Biology and Center for Cancer Research
    Howard Hughes Medical Institute)

Abstract

The tumour-suppressor gene p53 is frequently mutated in human cancers and is important in the cellular response to DNA damage1,2. Although the p53 family members p63 and p73 are structurally related to p53, they have not been directly linked to tumour suppression, although they have been implicated in apoptosis3,4,5,6,7,8,9. Given the similarity between this family of genes and the ability of p63 and p73 to transactivate p53 target genes10,11, we explore here their role in DNA damage-induced apoptosis. Mouse embryo fibroblasts deficient for one or a combination of p53 family members were sensitized to undergo apoptosis through the expression of the adenovirus E1A oncogene12,13,14. While using the E1A system facilitated our ability to perform biochemical analyses, we also examined the functions of p63 and p73 using an in vivo system in which apoptosis has been shown to be dependent on p53. Using both systems, we show here that the combined loss of p63 and p73 results in the failure of cells containing functional p53 to undergo apoptosis in response to DNA damage.

Suggested Citation

  • Elsa R. Flores & Kenneth Y. Tsai & Denise Crowley & Shomit Sengupta & Annie Yang & Frank McKeon & Tyler Jacks, 2002. "p63 and p73 are required for p53-dependent apoptosis in response to DNA damage," Nature, Nature, vol. 416(6880), pages 560-564, April.
  • Handle: RePEc:nat:nature:v:416:y:2002:i:6880:d:10.1038_416560a
    DOI: 10.1038/416560a
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/416560a
    File Function: Abstract
    Download Restriction: Access to the full text of the articles in this series is restricted.

    File URL: https://libkey.io/10.1038/416560a?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. Melanie Weigert & Yan Li & Lisha Zhu & Heather Eckart & Preety Bajwa & Rahul Krishnan & Sarah Ackroyd & Ricardo Lastra & Agnes Bilecz & Anindita Basu & Ernst Lengyel & Mengjie Chen, 2025. "A cell atlas of the human fallopian tube throughout the menstrual cycle and menopause," Nature Communications, Nature, vol. 16(1), pages 1-15, 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:416:y:2002:i:6880:d:10.1038_416560a. 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.