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Expression of beta-catenin is regulated by PI-3 kinase and sodium butyrate in colorectal cancer cells

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F05%3A00024289" target="_blank" >RIV/68378050:_____/05:00024289 - isvavai.cz</a>

  • Alternative codes found

    RIV/68378050:_____/06:00043549

  • Result on the web

  • DOI - Digital Object Identifier

Alternative languages

  • Result language

    angličtina

  • Original language name

    Expression of beta-catenin is regulated by PI-3 kinase and sodium butyrate in colorectal cancer cells

  • Original language description

    ?-catenin is implicated in intercellular junctions and transcriptional co-activation. Here we examined regulation of the expression of ?-catenin in HT29 colorectal adenocarcinoma cells. Our results showed that inhibition of PI-3 kinase with wortmannin was accompanied by a considerably reduced expression of ?-catenin. This effect was overcome by butyrate and occured at the protein level, not at the level of mRNA. Moreover, NaBT significantly increased phosphorylation of the ribosomal protein S6, participating in translational control of gene expression. This was accompanied by the increased phosphorylation of p70 S6K and MAPKs, the effector proteins that are upstream of protein S6 in the distinct signaling pathways. These facts indicate that different signaling pathways may be involved in the regulation of ?-catenin synthesis. Modulation of ?-catenin expression by NaBT occured at the level of protein translation, suggesting that NaBT may act as a translational regulator.

  • Czech name

    Exprese beta-kateninu je v kolorektálních nádorových buňkách regulována PI-3 kinázou a butyrátem sodným

  • Czech description

    ?-katenin se účastní mezibuněčných spojů a transkripční ko-aktivace. V této práci jsme studovali regulaci exprese ?-kateninu v buňkách kolorektálního adenokarcinomu HT29. Naše výsledky ukázaly, že inhibice PI-3 kinázy wortmanninem byla provázená značně zredukovanou expresí ?-kateninu. Tomuto účinku zabránil butyrát sodný na úrovni přepisu proteinu, nikoli mRNA. NaBT navíc znatelně zvýšil fosforylaci ribosomálního proteinu S6, který se podílí na kontrole translace. Zvýšila se také fosforylace p70 S6 kinázy a MAPK kináz, jež jsou členy dvou signálních drah vedoucích k aktivaci S6 proteinu. Tato fakta ukazují, že za regulaci tvorby ?-kateninu mohou zodpovídat dvě různé signální dráhy. Protože se regulace exprese ?-kateninu odehrála na úrovni translace proteinů, navrhujeme, že NaBT hraje roli translačního regulátoru. To odhaluje zcela novou funkci tohoto diferenciačního agens.

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

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

  • Continuities

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)<br>Z - Vyzkumny zamer (s odkazem do CEZ)

Others

  • Publication year

    2005

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    International Journal of Molecular Medicine

  • ISSN

    1107-3756

  • e-ISSN

  • Volume of the periodical

    17

  • Issue of the periodical within the volume

    1

  • Country of publishing house

    GR - GREECE

  • Number of pages

    7

  • Pages from-to

    69-75

  • UT code for WoS article

  • EID of the result in the Scopus database