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Or cells, which was due to the activation of ERK and p53. To the best of our knowledge, this is the first study to report the molecular mechanism of the chemotherapeutic effects of Triphala against pancreatic cancer. Reactive oxygen species (ROS) are the known mediators of intracellular signaling cascades. Excessive production of ROS nonetheless leads to oxidative stress, loss of cell function and
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Activation of ERK with induction of apoptosis by various chemopreventive and chemotherapeutic agents [39-41]. In fact, oxidants have been shown to activate ERK by taking over the growth factor receptor signaling pathways [42-46]. Moreover, ERK may get activated in response to DNA damage and can phosphorylate p53 in vitro [23,24,47-49]. We found that exposure of Capan-2 or BxPC-3 cells with apoptos
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Mail: Vinzenz Link - link@mpi-cbg.de; Andrej Shevchenko - shevchenko@mpi-cbg.de; Carl-Philipp Heisenberg* - heisenberg@mpi-cbg.de * Corresponding authorPublished: 13 January 2006 BMC Developmental Biology 2006, 6:1 doi:10.1186/1471-213X-6-Received: 28 August 2005 Accepted: 13 JanuaryThis article is available from: http://www.biomedcentral.com/1471-213X/6/1 ?2006 Link et al; licensee BioMed Central