Rat Hepatocyte Primary Cell Culture-Mediated Mutagenesis of Adult Rat Liver Epithelial Cells by Procarcinogens

1977 ◽  
Vol 156 (3) ◽  
pp. 534-538 ◽  
Author(s):  
R. H. C. San ◽  
G. M. Williams
2003 ◽  
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Author(s):  
Tamara Vanhaecke ◽  
Karen De Smet ◽  
Sonja Beken ◽  
Marleen Pauwels ◽  
Antoine Vercruysse ◽  
...  

Biochimie ◽  
1975 ◽  
Vol 56 (10) ◽  
pp. 1365-1379 ◽  
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Martine Chessebeuf ◽  
Aline Olsson ◽  
Paulette Bournot ◽  
Jean Desgres ◽  
Michel Guiguet ◽  
...  

2006 ◽  
pp. 239-246
Author(s):  
Tom Henkens ◽  
Tamara Vanhaecke ◽  
Peggy Papeleu ◽  
Greetje Elaut ◽  
Mathieu Vinken ◽  
...  

2005 ◽  
Vol 386 (3) ◽  
pp. 217-223 ◽  
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Kotb Abdelmohsen ◽  
Claudia von Montfort ◽  
Dominik Stuhlmann ◽  
P. Arne Gerber ◽  
Ulrich K.M. Decking ◽  
...  

Abstract Exposure of rat liver epithelial cells to doxorubicin, an anthraquinone derivative widely employed in cancer chemotherapy, led to a dose-dependent decrease in gap junctional intercellular communication (GJC). Gap junctions are clusters of inter-cellular channels consisting of connexins, the major connexin in the cells used being connexin-43 (Cx43). Doxorubicin-induced loss of GJC was mediated by activation of extracellular signal-regulated kinase (ERK)-1 and ERK-2, as demonstrated using inhibitors of ERK activation. Furthermore, activation of the epidermal growth factor (EGF) receptor by doxorubicin was responsible for ERK activation and the subsequent attenuation of GJC. Inhibition of GJC, however, was not by direct phosphorylation of Cx43 by ERK-1/2, whereas menadione, a 1,4-naphthoquinone derivative that was previously demonstrated to activate the same EGF receptor-dependent pathway as doxorubicin, resulting in downregulation of GJC, caused strong phos-phorylation of Cx43 at serines 279 and 282. Thus, ERK-dependent downregulation of GJC upon exposure to quinones may occur both by direct phosphorylation of Cx43 and in a phosphorylation-independent manner.


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