Number of the records: 1  

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

  1. 1.
    0394860 - BFÚ 2014 RIV US eng J - Journal Article
    Procházková, Jiřina - Kabátková, Markéta - Šmerdová, Lenka - Pachernik, J. - Sýkorová, D. - Kohoutek, J. - Šimečková, P. - Hrubá, E. - Kozubík, Alois - Machala, M. - Vondráček, Jan
    Aryl Hydrocarbon Receptor Negatively Regulates Expression of the Plakoglobin Gene (Jup).
    Toxicological Sciences. Roč. 134, č. 2 (2013), s. 258-270. ISSN 1096-6080. E-ISSN 1096-0929
    R&D Projects: GA ČR(CZ) GA524/09/1337; GA ČR(CZ) GD204/09/H058; GA MŠMT(CZ) EE2.3.30.0030
    Grant - others:GA ČR(CZ) GA301/09/1832
    Institutional research plan: CEZ:AV0Z50040702
    Institutional support: RVO:68081707
    Keywords : EMBRYONIC STEM-CELLS * LIVER EPITHELIAL-CELLS * AH RECEPTOR
    Subject RIV: BO - Biophysics
    Impact factor: 4.478, year: 2013

    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 Jup expression 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 stem cells, or cardiomyocytes isolated from neonatal rat hearts. The small interfering RNA (siRNA)mediated knockdown of AhR confirmed its role in both basal and TCDD-deregulated Jup expression.
    Permanent Link: http://hdl.handle.net/11104/0223042

     
     
Number of the records: 1  

  This site uses cookies to make them easier to browse. Learn more about how we use cookies.