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Gain-of-function mutations of PPM1D/Wip1 impair the p53-dependent G1 checkpoint

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11110%2F13%3A10192709" target="_blank" >RIV/00216208:11110/13:10192709 - isvavai.cz</a>

  • Alternative codes found

    RIV/68378050:_____/13:00423172 RIV/61989592:15110/13:33143841 RIV/00064165:_____/13:10192709

  • Result on the web

    <a href="http://dx.doi.org/10.1083/jcb.201210031" target="_blank" >http://dx.doi.org/10.1083/jcb.201210031</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1083/jcb.201210031" target="_blank" >10.1083/jcb.201210031</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Gain-of-function mutations of PPM1D/Wip1 impair the p53-dependent G1 checkpoint

  • Original language description

    The DNA damage response (DDR) pathway and its core component tumor suppressor p53 block cell cycle progression after genotoxic stress and represent an intrinsic barrier preventing cancer development. The serine/threonine phosphatase PPM1D/Wip1 inactivates p53 and promotes termination of the DDR pathway. Wip1 has been suggested to act as an oncogene in a subset of tumors that retain wild-type p53. In this paper, we have identified novel gain-of-function mutations in exon 6 of PPM1D that result in expression of C-terminally truncated Wip1. Remarkably, mutations in PPM1D are present not only in the tumors but also in other tissues of breast and colorectal cancer patients, indicating that they arise early in development or affect the germline. We show thatmutations in PPM1D affect the DDR pathway and propose that they could predispose to cancer.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

  • CEP classification

    FD - Oncology and haematology

  • OECD FORD branch

Result continuities

  • Project

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2013

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Journal of Cell Biology

  • ISSN

    0021-9525

  • e-ISSN

  • Volume of the periodical

    201

  • Issue of the periodical within the volume

    4

  • Country of publishing house

    GB - UNITED KINGDOM

  • Number of pages

    11

  • Pages from-to

    511-521

  • UT code for WoS article

    000318909500005

  • EID of the result in the Scopus database