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Statements

Subject Item
n2:RIV%2F00027162%3A_____%2F07%3A%230000283%21RIV08-MZE-00027162
rdf:type
skos:Concept n10:Vysledek
dcterms:description
Různé jaterní choroby vedou k rozsáhlé zánětlivé odpovědi a uvolnění řady prozánětlivých cytokinů, jako je TNF-alfa. Zabývali jsme se možnými interakcemi TNF-alfa s ligandy receptoru AhR a známými jaterními karcinogeny, jako je 2,3,7,8-TCDD a koplanární PCB 126. TNF-alfa významně zesiloval proliferační účinky pikomolárních koncentrací TCDD i PCB 126, což vedlo k nárustu počtu buněk a zvýšenému procentu buněk vstupujících do S-fáze buněčného cyklu. Kombinace TNF-alfa s nízkými koncentracemi ligandů AhR zvyšovala hladinu cyklinu A na úrovni mRNA i proteinu. TNF-alfa dočasně inhiboval AhR-dependentní indukci cytochromu 1A1. Naproti tomu, TNF-alfa významně zvyšoval indukci CYP1B1. Tyto výsledky naznačují, že TNF-alfa může významně zesilovat účinky ligandů AhR na deregulaci kontroly buněčné proliferace, stejně jako účinky na expresi CYP1B1, který je zahrnut v metabolické aktivaci řady mutagenních sloučenin. Various liver diseases lead to an extensive inflammatory response and release of pro-inflammatory cytokines, such as TNF-alpha. We investigated possible interactions of TNF-alpha with ligands of the AhR receptor and known liver carcinogens, such as 2,3,7,8-TCDD and co-planar PCB 126. TNF-alpha significantly potentiated proliferative effects of picomolar range doses of both TCDD and PCB 126, leading to an increase in cell numbers, as well as an increased percentage of cells entering the S-phase of the cell cycle. The combination of TNF-alpha with low concentrations of AhR ligands increased both mRNA and protein levels of cyclin A. TNF-alpha temporarily inhibited AhR-dependent induction of CYP1A1. In contrast, TNF-alpha significantly enhanced induction of CYP1B1. These results suggest that TNF-alpha can significantly amplify effects of AhR ligands on deregulation of cell proliferation control, as well as on expression of CYP1B1, involved in metabolic activation of a number of mutagenic compounds. Various liver diseases lead to an extensive inflammatory response and release of pro-inflammatory cytokines, such as TNF-alpha. We investigated possible interactions of TNF-alpha with ligands of the AhR receptor and known liver carcinogens, such as 2,3,7,8-TCDD and co-planar PCB 126. TNF-alpha significantly potentiated proliferative effects of picomolar range doses of both TCDD and PCB 126, leading to an increase in cell numbers, as well as an increased percentage of cells entering the S-phase of the cell cycle. The combination of TNF-alpha with low concentrations of AhR ligands increased both mRNA and protein levels of cyclin A. TNF-alpha temporarily inhibited AhR-dependent induction of CYP1A1. In contrast, TNF-alpha significantly enhanced induction of CYP1B1. These results suggest that TNF-alpha can significantly amplify effects of AhR ligands on deregulation of cell proliferation control, as well as on expression of CYP1B1, involved in metabolic activation of a number of mutagenic compounds.
dcterms:title
Tumor necrosis factor-alpha modulates effects of aryl hydrocarbon receptor ligands on cell proliferation and expression of cytochrome P450 enzymes in rat liver 'stem-like' cells TNF-alfa moduluje efekty ligandů receptoru AhR na buněčnou proliferaci a expresi enzymů cytochromů P450 v potkaních jaterních 'stem-like' buňkách Tumor necrosis factor-alpha modulates effects of aryl hydrocarbon receptor ligands on cell proliferation and expression of cytochrome P450 enzymes in rat liver 'stem-like' cells
skos:prefLabel
Tumor necrosis factor-alpha modulates effects of aryl hydrocarbon receptor ligands on cell proliferation and expression of cytochrome P450 enzymes in rat liver 'stem-like' cells Tumor necrosis factor-alpha modulates effects of aryl hydrocarbon receptor ligands on cell proliferation and expression of cytochrome P450 enzymes in rat liver 'stem-like' cells TNF-alfa moduluje efekty ligandů receptoru AhR na buněčnou proliferaci a expresi enzymů cytochromů P450 v potkaních jaterních 'stem-like' buňkách
skos:notation
RIV/00027162:_____/07:#0000283!RIV08-MZE-00027162
n4:strany
79;89
n4:aktivita
n17:Z
n4:aktivity
Z(MZE0002716201)
n4:cisloPeriodika
1
n4:dodaniDat
n6:2008
n4:domaciTvurceVysledku
n5:2499304 n5:4628713 n5:3547884 n5:2301229 n5:5686350
n4:druhVysledku
n11:J
n4:duvernostUdaju
n8:S
n4:entitaPredkladatele
n14:predkladatel
n4:idSjednocenehoVysledku
455973
n4:idVysledku
RIV/00027162:_____/07:#0000283
n4:jazykVysledku
n15:eng
n4:klicovaSlova
cell proliferation; tumor necrosis factor-alpha; aryl hydrocarbon receptor; polychlorinated biphenyl; dioxin; xenobiotic metabolizing enzymes
n4:klicoveSlovo
n7:tumor%20necrosis%20factor-alpha n7:dioxin n7:polychlorinated%20biphenyl n7:xenobiotic%20metabolizing%20enzymes n7:aryl%20hydrocarbon%20receptor n7:cell%20proliferation
n4:kodStatuVydavatele
GB - Spojené království Velké Británie a Severního Irska
n4:kontrolniKodProRIV
[B6D11F2E53F2]
n4:nazevZdroje
Toxicological Sciences
n4:obor
n16:EB
n4:pocetDomacichTvurcuVysledku
5
n4:pocetTvurcuVysledku
8
n4:rokUplatneniVysledku
n6:2007
n4:svazekPeriodika
99
n4:tvurceVysledku
Machala, Miroslav Vondráček, Jan Májková, Z. Hennig, B. Kozubík, A. Umannová, Lenka Krčmář, Pavel Zatloukalová, Jiřina
n4:zamer
n13:MZE0002716201
s:issn
1096-6080
s:numberOfPages
11