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Transforming growth factor-beta1 inhibits all-trans retinoic acid-induced apoptosis

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68081707%3A_____%2F06%3A00039016" target="_blank" >RIV/68081707:_____/06:00039016 - isvavai.cz</a>

  • Alternative codes found

    RIV/00216208:11130/06:2942

  • Result on the web

  • DOI - Digital Object Identifier

Alternative languages

  • Result language

    angličtina

  • Original language name

    Transforming growth factor-beta1 inhibits all-trans retinoic acid-induced apoptosis

  • Original language description

    The interaction between retinoids and transforming growth factor-beta1 (TGF-beta1) leading to regulation of proliferation, differentiation and apoptosis is not still fully understood. In this study, we demonstrated that a combination treatment with all-trans retinoic acid (ATRA) and TGF-beta1 led to the enhancement of ATRA-induced suppression of cell proliferation, which is accompanied by inhibition of ATRA-induced apoptosis in human leukemia HL-60 cells. Inhibition of ATRA-induced apoptosis by TGF-beta1 was associated with an increased level of Mcl-l protein, but not with inhibition of mitochondrial membrane depolarization. Upregulation of c-FLIPL protein, an inhibitor of apoptosis induced by TRAIL, correspond with inhibition of caspase-8 activation.In summary, we demonstrate that the balance of processes leading to regulation of proliferation and differentiation of myeloid cells can modulate cell sensitivity to apoptosis-inducing stimuli.

  • Czech name

    Transformující růstový faktor beta1 inhibuje apoptózu indukovanou kyselinou retinovou

  • Czech description

    Interakce mezi působením retinoidů a transformujícího růstového faktoru - beta1 (TGF-beta1) která vede k regulaci proliferace, diferenciace a apoptózy není stále plně objasněna. V této práci jsme prokázali, že kombinované působení kyseliny retinové (ATRA) a TGF-beta1 vedlo k inhibici apoptózy indukované ATRA u lidských leukemických buněk HL-60. Inhibice apoptózy indukované ATRA byla provázena zvýšením exprese proteinu Mcl-l, ale ne s inhibicí depolarizace mitochondirálního potenciálu. Zvýšená exprese c-FLIPL proteinu, který je inhibitorem apoptózy indukované TRAIL(em) korelovala s inhibicí aktivace kaspázy-8. Prokázali jsme, že rovnováha mezi procesy vedoucími k regulaci proliferace a diferenciace u myeloidních buněk může modulovat citlivost ke stimulům indukujícím apoptózu.

Classification

  • Type

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

  • CEP classification

    BO - Biophysics

  • 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

    2006

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    Leukemia Research

  • ISSN

    0145-2126

  • e-ISSN

  • Volume of the periodical

    30

  • Issue of the periodical within the volume

    5

  • Country of publishing house

    GB - UNITED KINGDOM

  • Number of pages

    17

  • Pages from-to

    607-623

  • UT code for WoS article

  • EID of the result in the Scopus database