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

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About: The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid Goto Sponge NotDistinct Permalink

An Entity of Type : http://linked.opendata.cz/ontology/domain/vavai/Vysledek, within Data Space : linked.opendata.cz associated with source document(s)

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rdf:type	skos:Concept http://linked.opendata.cz/ontology/domain/vavai/Vysledek
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 RAR 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 as biological 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 proliferation, differentiation, and apoptosis. These experiments showed that EVI1 modulated the ATRA response of several dozens of genes, and in fact reinforced it in the vast majority of cases. 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 RAR 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 as biological 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 proliferation, differentiation, and apoptosis. These experiments showed that EVI1 modulated the ATRA response of several dozens of genes, and in fact reinforced it in the vast majority of cases. (en)
Title	The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid (en)
skos:prefLabel	The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid (en)
skos:notation	RIV/68081707:_____/14:00441294!RIV15-AV0-68081707
http://linked.open...avai/riv/aktivita	I P
http://linked.open...avai/riv/aktivity	I, P(ED1.100/02/0123)
http://linked.open...iv/cisloPeriodika	18
http://linked.open...vai/riv/dodaniDat	2015
http://linked.open...aciTvurceVysledku	Slabáková, Eva Souček, Karel
http://linked.open.../riv/druhVysledku	J - Článek v odborném periodiku
http://linked.open...iv/duvernostUdaju	S - Úplné a pravdivé údaje nepodléhající ochraně podle zvláštních právních předpisů
http://linked.open...titaPredkladatele	Biofyzikální ústav AV ČR, v. v. i.
http://linked.open...dnocenehoVysledku	34552
http://linked.open...ai/riv/idVysledku	RIV/68081707:_____/14:00441294
http://linked.open...riv/jazykVysledku	eng - angličtina
http://linked.open.../riv/klicovaSlova	apoptosis; cell cycle; EVI1 (en)
http://linked.open.../riv/klicoveSlovo	apoptosis EVI1 cell cycle
http://linked.open...odStatuVydavatele	US - Spojené státy americké
http://linked.open...ontrolniKodProRIV	[7C282B9E09C5]
http://linked.open...i/riv/nazevZdroje	Cell Cycle
http://linked.open...in/vavai/riv/obor	BO
http://linked.open...ichTvurcuVysledku	2 (xsd:int)
http://linked.open...cetTvurcuVysledku	10 (xsd:int)
http://linked.open...vavai/riv/projekt	St. Anne´s University Hospital Brno - International Clinical Research Center (FNUSA-ICRC)
http://linked.open...UplatneniVysledku	2014
http://linked.open...v/svazekPeriodika	13
http://linked.open...iv/tvurceVysledku	Slabáková, Eva Souček, Karel Arbesu, I. Hackl, H. Schwarzinger, I. Shehata, M. Smějová, M. Spittler, A. Steinmetz, B. Wieser, R.
http://linked.open...ain/vavai/riv/wos	000348325800020
issn	1538-4101
number of pages	13 (xsd:int)

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