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Endoplasmic reticulum stress sensitizes cells to DNA damage-induced apoptosis through p53-dependent suppression of CDKN1A

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00209805%3A_____%2F14%3A%230000562" target="_blank" >RIV/00209805:_____/14:#0000562 - isvavai.cz</a>

  • Result on the web

    <a href="http://www.nature.com/ncomms/2014/141008/ncomms6067/full/ncomms6067.html" target="_blank" >http://www.nature.com/ncomms/2014/141008/ncomms6067/full/ncomms6067.html</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1038/ncomms6067" target="_blank" >10.1038/ncomms6067</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Endoplasmic reticulum stress sensitizes cells to DNA damage-induced apoptosis through p53-dependent suppression of CDKN1A

  • Original language description

    Endoplasmic reticulum (ER) stress occurs in poorly perfused tissues and activates the p53 isoform p53/47 to promote G2 arrest via 14-3-3s. This contrasts with the p21CDKN1A-dependent G1 arrest caused by p53 following DNA damage. It is not known how cellsrespond to conditions when both pathways are activated. Here we show that p53/47 prevents p53-induced p21 transcription during ER stress and that both isoforms repress p21 mRNA translation. This prevents p21 from promoting constitutive photomorphogenic1-mediated 14-3-3s degradation and leads to G2 arrest. DNA damage does not result in p53-dependent induction of p21 during ER stress and instead results in an increase in p53-induced apoptosis. This illustrates how p53 isoforms target an intrinsic balance between the G1 and G2 checkpoints for cell cycle coordination and demonstrates an ER stress-dependent p53 pathway that suppresses p21 and lowers the apoptotic threshold to genotoxic drugs.

  • Czech name

  • Czech description

Classification

  • Type

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

  • CEP classification

    EB - Genetics and molecular biology

  • OECD FORD branch

Result continuities

  • Project

    <a href="/en/project/ED2.1.00%2F03.0101" target="_blank" >ED2.1.00/03.0101: Regional Centre for Applied Molecular Oncology (RECAMO)</a><br>

  • Continuities

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Others

  • Publication year

    2014

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    Nature communications

  • ISSN

    2041-1723

  • e-ISSN

  • Volume of the periodical

    5

  • Issue of the periodical within the volume

    8 October

  • Country of publishing house

    GB - UNITED KINGDOM

  • Number of pages

    16

  • Pages from-to

    5067

  • UT code for WoS article

    000343977100002

  • EID of the result in the Scopus database