scholarly journals A3Adenosine Receptor Activation Inhibits Cell Proliferation via Phosphatidylinositol 3-Kinase/Akt-dependent Inhibition of the Extracellular Signal-regulated Kinase 1/2 Phosphorylation in A375 Human Melanoma Cells

2005 ◽  
Vol 280 (20) ◽  
pp. 19516-19526 ◽  
Author(s):  
Stefania Merighi ◽  
Annalisa Benini ◽  
Prisco Mirandola ◽  
Stefania Gessi ◽  
Katia Varani ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Receptor Activation ◽  
Melanoma Cells ◽  
Human Melanoma ◽  
Phosphatidylinositol 3 Kinase ◽  
Extracellular Signal Regulated Kinase ◽  
Human Melanoma Cells ◽  
Extracellular Signal ◽  
Dependent Inhibition ◽  
Phosphatidylinositol 3

Contribution of phosphatidylinositol 3-kinase to radiation resistance in human melanoma cells

1999 ◽  
Vol 24 (1) ◽  
pp. 64-69 ◽  
Author(s):  
Mikhail Krasilnikov ◽  
Victor Adler ◽  
Serge Y. Fuchs ◽  
Zheng Dong ◽  
Adriana Haimovitz-Friedman ◽  
...  
Keyword(s):  
Radiation Resistance ◽  
Melanoma Cells ◽  
Human Melanoma ◽  
Phosphatidylinositol 3 Kinase ◽  
Human Melanoma Cells ◽  
Phosphatidylinositol 3

The effect of TGF-β1 on cell proliferation and proteoglycan production in human melanoma cells depends on the degree of cell differentiation

1996 ◽  
Vol 109 (1-2) ◽  
pp. 39-47 ◽  
Author(s):  
Ascensión Heredia ◽  
Juan Villena ◽  
Manuel Romarís ◽  
Anna Molist ◽  
Anna Bassols
Keyword(s):  
Cell Proliferation ◽  
Cell Differentiation ◽  
Melanoma Cells ◽  
Human Melanoma ◽  
Human Melanoma Cells ◽  
Tgf Β1

Control of intracellular calcium by membrane potential in human melanoma cells

1993 ◽  
Vol 265 (6) ◽  
pp. C1501-C1510 ◽  
Author(s):  
B. Nilius ◽  
G. Schwarz ◽  
G. Droogmans
Keyword(s):  
Cell Proliferation ◽  
Membrane Potential ◽  
Intracellular Calcium ◽  
Reversal Potential ◽  
Melanoma Cells ◽  
Human Melanoma ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Patch Clamp Technique ◽  
Human Melanoma Cells

The modulation of intracellular calcium ([Ca2+]i) by the membrane potential was investigated in human melanoma cells by combining the nystatin-perforated patch-clamp technique with Ca2+ measurements. Voltage steps to -100 mV induced a rise in [Ca2+]i and a creeping inward current. These effects were absent in Ca(2+)-free solution and could be blocked by Ni2+ or La3+. Voltage ramps revealed a close correlation between [Ca2+]i and voltage, with the strongest voltage dependence around the resting potential. Long-lasting tail currents, closely correlated with the rise in [Ca2+]i and a reversal potential close to the K+ equilibrium potential, occurred if the membrane potential was clamped back to 0 mV. They were absent if intracellular K+ was replaced by Cs+ and blocked by extracellular tetraethylammonium (5 mM), Ba2+ (1 mM), or a membrane-permeable adenosine 3',5'-cyclic monophosphate analogue. These observations are discussed in relation to cell proliferation. The enhanced expression of K+ channels during cell proliferation provides a positive-feedback mechanism resulting in long-term changes in [Ca2+]i required for the G1-S transition in the cell cycle.

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