scholarly journals Polo-like kinase 1 inhibitors SBE13 and BI 2536 induce different responses in primary cells

Cell Cycle ◽  
2011 ◽  
Vol 10 (7) ◽  
pp. 1031-1030 ◽  
Author(s):  
Frank Eckerdt
Keyword(s):  
Pneumologie ◽  
2009 ◽  
Vol 63 (S 01) ◽  
Author(s):  
M Sebastian ◽  
M Reck ◽  
J von Pawel ◽  
W Digel ◽  
G Ay ◽  
...  
Keyword(s):  

2010 ◽  
Vol 48 (08) ◽  
Author(s):  
S Thrum ◽  
J Lorenz ◽  
J Mössner ◽  
M Wiedmann
Keyword(s):  

2007 ◽  
Vol 45 (01) ◽  
Author(s):  
T Speicher ◽  
G Künstle ◽  
A Wendel

2014 ◽  
Vol 14 (5) ◽  
pp. 365-376 ◽  
Author(s):  
Abarrategui-Pontes Cecilia ◽  
Creneguy Alison ◽  
Thinard Reynald ◽  
Fine J. ◽  
Thepenier Virginie ◽  
...  

1988 ◽  
Vol 255 (4) ◽  
pp. E469-E474
Author(s):  
J. P. Kile ◽  
M. S. Amoss

It has been proposed that gonadotropin-releasing hormone (GnRH) stimulates Ca2+ entry by activation of voltage-independent, receptor-mediated Ca2+ channels in the rat gonadotroph. Little work has been done on the role of calcium in GnRH-induced luteinizing hormone (LH) release in species other than the rat. Therefore, this study was done to compare the effects of agents that alter Ca2+ or Na+ entry on LH release from calf anterior pituitary primary cells in culture. GnRH (100 ng/ml), Ca2+ ionophore A23187 (2.5 microM), and the depolarizing agent ouabain (0.1-10 microM) all produced significant increases (P less than 0.05) in LH release; these effects were significantly reduced when the cells were preincubated with the organic Ca2+ channel blockers nifedipine (1-10 microM) and verapamil (1-10 microM) and with Co2+ (0.01-1 mM). The effect of ouabain was inhibited by tetrodotoxin (TTX; 1-10 nM) as well as by nifedipine at 0.1-10 microM. In contrast to its effect on rat pituitary LH release, TTX significantly inhibited GnRH-stimulated LH release at 1-100 nM. These results suggest that GnRH-induced LH release may employ Ca2+ as a second messenger in bovine gonadotrophs and support recent speculation that GnRH-induced Ca2+ mobilization may in part be voltage dependent.


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