All

What are you looking for?

All
Projects
Results
Organizations

Quick search

  • Projects supported by TA ČR
  • Excellent projects
  • Projects with the highest public support
  • Current projects

Smart search

  • That is how I find a specific +word
  • That is how I leave the -word out of the results
  • “That is how I can find the whole phrase”

Activation of DNA binding ability of latent p53 protein by protein kinase C is abolished by casein kinase II

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00209805%3A_____%2F04%3A00013927" target="_blank" >RIV/00209805:_____/04:00013927 - isvavai.cz</a>

  • Result on the web

  • DOI - Digital Object Identifier

Alternative languages

  • Result language

    angličtina

  • Original language name

    Activation of DNA binding ability of latent p53 protein by protein kinase C is abolished by casein kinase II

  • Original language description

    We found that phosphorylation of p53 by CK2 on Ser392 induces its DNA binding aktivity of p53 to a much lower extent than phosphorylation by cdk2/cyclin A or PKC. In addition, we found that phosphorylation by CK2 strongly inhibits PKC-induced activationof p53 DNA binding, while the activation of p53 by cdk2/cyclin A is not affected by CK2. The presence of CK2-mediated phosphorylation promotes PKC binding to its docking site within the p53 oligomerization domain, but decreases phosphorylation of p53 byPKC, suggesting that competition between CK2 and PKC does not rely on the inhibition of PKC?p53 complex formation. These results indicate the crucial role of p53 C-terminal phosphorylation in the regulation of its DNA-binding activity, but also suggest that antagonistic relationships exist between different stress signalling pathways.

  • Czech name

    Aktivace DNA vazebne schopnosti latentni formy p53 protin kinasou C je inhibovana kasein kinasou II

  • Czech description

    Zjistili jsme že fosforylace p53 CK2 na Ser392 indukuje DNA vazebnou aktivitu p53 mnohem méně než fosforylace cdk2/cyclin A nebo PKC. Navíc jsme zjistili, že fosforylace CK2 silně inhibuje PKC indukovanou aktivaci vazby p53 na DNA, zatímco aktivace p53 cdk2/cyclin A není ovlivněna. Fosforylace CK2 zvyšuje vazbu PKC do jejího vazebného místa v p53 oligomerizační doméně, ale přitom snižuje fosforylaci p53 PKC. Tento poznatek potvrzuje, že kompetici mezi CK2 a PKC není závislá na inhibici tvorby komplexu p53-PKC. Tyto výsledky potvrzují důležitost C-koncové fosforylace při regulaci DNA vazebné aktivity proteinu p53 a současně potvrzují antagonistický vztah existující mezi rozdílnými stresovými drahami.

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

    <a href="/en/project/GA301%2F02%2F0831" target="_blank" >GA301/02/0831: Interactions of p53 protein and its homologues with DNA and their role in malignant transformation</a><br>

  • Continuities

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

Others

  • Publication year

    2004

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    The Biochemical journal

  • ISSN

    0264-6021

  • e-ISSN

  • Volume of the periodical

    378

  • Issue of the periodical within the volume

    pt. 3

  • Country of publishing house

    GB - UNITED KINGDOM

  • Number of pages

    9

  • Pages from-to

    939-947

  • UT code for WoS article

  • EID of the result in the Scopus database