The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid
The result's identifiers
Result code in 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>
Alternative codes found
RIV/68081707:_____/14:00441294 RIV/00216224:14310/14:00107098
Result on the web
<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>
Alternative languages
Result language
angličtina
Original language name
The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid
Original language description
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
Czech name
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Czech description
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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
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Result continuities
Project
<a href="/en/project/ED1.100%2F02%2F0123" target="_blank" >ED1.100/02/0123: St. Anne´s University Hospital Brno - International Clinical Research Center (FNUSA-ICRC)</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
Cell Cycle
ISSN
1538-4101
e-ISSN
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Volume of the periodical
13
Issue of the periodical within the volume
18
Country of publishing house
US - UNITED STATES
Number of pages
13
Pages from-to
2931-2943
UT code for WoS article
000348325800020
EID of the result in the Scopus database
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