. "6"^^ . "1550"^^ . . . "0"^^ . . "6"^^ . "Polycyklick\u00E9 aromatick\u00E9 uhlovod\u00EDky (PAU pat\u0159\u00ED mezi environment\u00E1ln\u00ED faktory, kter\u00E9 mohou hr\u00E1t roli v rozvoji n\u00E1dorov\u00FDch onemocn\u011Bn\u00ED \u010Di reproduk\u010Dn\u00EDch a imunitn\u00EDch poruch. C\u00EDlem navrhovan\u00E9ho projektu je ov\u011B\u0159it hypot\u00E9zu, \u017Ee vliv PAU na bun\u011B\u010Dnou proliferaci/apopt\u00F3zu m\u016F\u017Ee b\u00FDt d\u00E1n jak akumulac\u00ED a aktivac\u00ED n\u00E1dorov\u00E9ho supresoru p53 v d\u016Fsledku genetoxick\u00E9ho stresu, tak aktivac\u00ED Ah receptoru (AhR), kter\u00FD by mohl m\u00EDt v\u00FDznam pro regulaci kontaktn\u00ED inhibice. Projekt bude zam\u011B\u0159en na detekci hladin (aktivity) p53 a PhR v in vitro bun\u011B\u010Dn\u00E9m modelu pro expozici souborem PAU, vybran\u00FDch na z\u00E1klad\u011B jejich vlivu na bun\u011B\u010Dnou proliferaci/apopt\u00F3zu. \u00DA\u010Dinky na kontaktn\u00ED inhibici budou porovn\u00E1v\u00E1ny s hladinami kl\u00ED\u010Dov\u00FDch protein\u016F typu kadherin\u016F a katenin\u016F po p\u016Fsoben\u00ED PAU, kter\u00E9 se pod\u00EDl\u00ED na regulaci mezibun\u011B\u010Dn\u00E9 adheze. C\u00EDlem je zjistit mo\u017En\u00FD vztah mezi zm\u011Bnami jejich exprese a vlivem PAU na bun\u011B\u010Dnou proliferaci."@cs . . . . "1"^^ . "1550"^^ . . . "Interactions of genotoxic and non-genotoxic effects of polycyclic aromatic hydrocarbons in regulation of cell proliferation"@en . "Interakce genotoxick\u00FDch a negenotoxick\u00FDch \u00FA\u010Dink\u016F polycyklick\u00FDch aromatick\u00FDch uhlovod\u00EDk\u016F v regulaci bun\u011B\u010Dn\u00E9 proliferace"@cs . . "polycyclic aromatic hydrocarbons; Ah receptor; p53; carcinogenesis; contact inhibition"@en . . "0"^^ . "Polycyclic aromatic hydrocarbons (PAHs) are among environmental factors known to play important roles in ethiology of cancer, reproductive or immune dysfunctions. The proposed project aims to test the hypothesis that ultimate fate of cells affected by PAH exposure might be determined both by accumulation and activation of p53 tumor suppressor induced by genotoxic stress, and the ligand-dependent activation of the aryl hydrocarbon receptor (AhR), which might play a role in regulation of contact inhibition. The project will focus on detection of p53 and PhR levels (and/or activation) in vitro after exposure to a set of PAHs, selected on basis of effects on cell proliferation/apoptosis. Effects on contact inhibition will be compared with levels of key catenin and cadherin proteins involved in formation of cell-to-cell adhesion following PAH exposure. The project aimt to investigate a relationship between changes in their expression and effects of PAHs on contact inhibition."@en .