Aryl Hydrocarbon Receptor Negatively Regulates Expression of the Plakoglobin Gene (Jup)

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00027162%3A_____%2F13%3A%230001035" target="_blank" >RIV/00027162:_____/13:#0001035 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/68081707:_____/13:00394860 RIV/00216224:14310/13:00080571

Výsledek na webu

<a href="http://dx.doi.org/10.1093/toxsci/kft110" target="_blank" >http://dx.doi.org/10.1093/toxsci/kft110</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1093/toxsci/kft110" target="_blank" >10.1093/toxsci/kft110</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Aryl Hydrocarbon Receptor Negatively Regulates Expression of the Plakoglobin Gene (Jup)

Popis výsledku v původním jazyce

Plakoglobin is an important component of intercellular junctions, including both desmosomes and adherens junctions, which is known as a tumor suppressor. Although mutations in the plakoglobin gene (Jup) and/or changes in its protein levels have been observed in various disease states, including cancer progression or cardiovascular defects, the information about endogenous or exogenous stimuli orchestrating Jup expression is limited. Here we show that the aryl hydrocarbon receptor (AhR) may regulate Jupexpression in a cell-specific manner. We observed a significant suppressive effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a model toxic exogenous activator of the AhR signaling, on Jup expression in a variety of experimental models derived from rodent tissues, including contact-inhibited rat liver progenitor cells (where TCDD induces cell proliferation), rat and mouse hepatoma cell models (where TCDD inhibits cell cycle progression), cardiac cells derived from the mouse embryonic

Název v anglickém jazyce

Aryl Hydrocarbon Receptor Negatively Regulates Expression of the Plakoglobin Gene (Jup)

Popis výsledku anglicky

Plakoglobin is an important component of intercellular junctions, including both desmosomes and adherens junctions, which is known as a tumor suppressor. Although mutations in the plakoglobin gene (Jup) and/or changes in its protein levels have been observed in various disease states, including cancer progression or cardiovascular defects, the information about endogenous or exogenous stimuli orchestrating Jup expression is limited. Here we show that the aryl hydrocarbon receptor (AhR) may regulate Jupexpression in a cell-specific manner. We observed a significant suppressive effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a model toxic exogenous activator of the AhR signaling, on Jup expression in a variety of experimental models derived from rodent tissues, including contact-inhibited rat liver progenitor cells (where TCDD induces cell proliferation), rat and mouse hepatoma cell models (where TCDD inhibits cell cycle progression), cardiac cells derived from the mouse embryonic

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

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

Z - Vyzkumny zamer (s odkazem do CEZ)

Rok uplatnění

2013

Kód důvěrnosti údajů

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

Název periodika

TOXICOLOGICAL SCIENCES

ISSN

1096-6080

e-ISSN

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Svazek periodika

134

Číslo periodika v rámci svazku

2

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

13

Strana od-do

258-270

Kód UT WoS článku

000322020300004

EID výsledku v databázi Scopus

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