The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00159816%3A_____%2F14%3A00061230" target="_blank" >RIV/00159816:_____/14:00061230 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/68081707:_____/14:00441294 RIV/00216224:14310/14:00107098

Výsledek na webu

<a href="http://dx.doi.org/10.4161/15384101.2014.946869" target="_blank" >http://dx.doi.org/10.4161/15384101.2014.946869</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.4161/15384101.2014.946869" target="_blank" >10.4161/15384101.2014.946869</a>

Jazyk výsledku

angličtina

Název v původním jazyce

The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid

Popis výsledku v původním jazyce

The product of the ecotropic virus integration site 1 (EVI1) gene, whose overexpression is associated with a poor prognosis in myeloid leukemias and some epithelial tumors, regulates gene transcription both through direct DNA binding and through modulation of the activity of other sequence specific transcription factors. Previous results from our laboratory have shown that EVI1 influenced transcription regulation in response to the myeloid differentiation inducing agent, all-trans retinoic acid (ATRA),in a dual manner: it enhanced ATRA induced transcription of the RARbeta gene, but repressed the ATRA induction of the EVI1 gene itself. In the present study, we asked whether EVI1 would modulate the ATRA regulation of a larger number of genes, as well asbiological responses to this agent, in human myeloid cells. U937 and HL-60 cells ectopically expressing EVI1 through retroviral transduction were subjected to microarray based gene expression analysis, and to assays measuring cellular pr

Název v anglickém jazyce

The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid

Popis výsledku anglicky

The product of the ecotropic virus integration site 1 (EVI1) gene, whose overexpression is associated with a poor prognosis in myeloid leukemias and some epithelial tumors, regulates gene transcription both through direct DNA binding and through modulation of the activity of other sequence specific transcription factors. Previous results from our laboratory have shown that EVI1 influenced transcription regulation in response to the myeloid differentiation inducing agent, all-trans retinoic acid (ATRA),in a dual manner: it enhanced ATRA induced transcription of the RARbeta gene, but repressed the ATRA induction of the EVI1 gene itself. In the present study, we asked whether EVI1 would modulate the ATRA regulation of a larger number of genes, as well asbiological responses to this agent, in human myeloid cells. U937 and HL-60 cells ectopically expressing EVI1 through retroviral transduction were subjected to microarray based gene expression analysis, and to assays measuring cellular pr

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

EB - Genetika a molekulární biologie

OECD FORD obor

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Projekt

<a href="/cs/project/ED1.100%2F02%2F0123" target="_blank" >ED1.100/02/0123: Fakultní nemocnice u sv. Anny v Brně - Mezinárodní centrum klinického výzkumu (FNUSA - ICRC)</a><br>

Návaznosti

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

Rok uplatnění

2014

Kód důvěrnosti údajů

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

Název periodika

Cell Cycle

ISSN

1538-4101

e-ISSN

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Svazek periodika

13

Číslo periodika v rámci svazku

18

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

13

Strana od-do

2931-2943

Kód UT WoS článku

000348325800020

EID výsledku v databázi Scopus

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