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Effects of Intracellular Calcium on Cell Survival and the MAPK Pathway in a Human Hormone-Dependent Leukemia Cell Line (TF-1)
aMembrane Research Group of the Hungarian Academy of Sciences, Nádor u. 7, H-1051 Budapest, Hungary bDepartment of Cell Metabolism, National Medical Center, Budapest, Hungary cInstitute of Enzymology, Hungarian Academy of Sciences, Budapest, Hungary
Address for correspondence: Ágota Apáti, Membrane Research Group of the Hungarian Academy of Sciences, Nádor u. 7, H-1051 Budapest, Hungary. apati{at}biomembrane.hu Ann. N.Y. Acad. Sci. 1010: 70-73 (2003).
Changes in the cytoplasmic calcium concentration ([Ca2+]i) regulate a wide variety of cellular processes. Here we demonstrate that increased [Ca2+]i was able to induce hormone-independent survival and proliferation, as well as to evoke apoptosis in human myelo-erythroid GM-CSF/IL-3 dependent leukemia cells (TF-1). Cellular responses induced by elevated [Ca2+]i depended on the duration and amplitude of the calcium-signal. Moderate or high, but transient, elevation of [Ca2+]i caused a transient, biphasic activation of ERK1/2 and protected cells from hormone withdrawal-induced apoptosis.1 In contrast, high and long-lasting elevation of [Ca2+]i led to sustained activation of the ERK1/2 kinases and apoptosis of TF-1 cells. Our data suggest that a time-dependent action of the MAPK pathway works as a decision-point between cell proliferation and apoptosis.
Key Words: cytoplasmic calcium concentration • ERK1/2 • c-Fos This article has been cited by other articles:
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