Cross-talks between c-Kit and PKC isoforms in HMC-1560 and HMC-1560,816 cells. Different role of PKCd in each cellular line

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Elsevier
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The c-kit inhibitor STI571 represents one of the most important treatments for patients with mastocytosis. However, intracellular pathways modulated by this compound are not completely defined. Here, STI571 effect on Protein Kinase C (PKC) regulation is determined in HMC-1 mast cell lines. STI571 activates PKCδ isoform resulting in HMC-1560 apoptosis. The apoptosis observed is PKCδ-dependent, since PKCδ-silencing avoids STI571 effect. c-kit inhibition implies nuclear PKCδ translocation characterized by a clear dependence on actin cytoskeleton integrity in HMC-1560 cell line, but not in HMC-1560,816. Therefore, PKCδ modulations can lead to a serious decrease in STI571 treatment-effectiveness

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Cellular Immunology (293) 2 (2015) Pages 104-112

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The research leading to these results has received funding from the following FEDER cofunded-grants. From CDTI and Technological Funds, supported by Ministerio de Economía y Competitividad, AGL2012-40185-CO2-01 and Consellería de Cultura, Educación e Ordenación Universitaria, GRC2013-016, and through Axencia Galega de Innovación, Spain, ITC-20133020 SINTOX, IN852A 2013/16-3 MYTIGAL. From CDTI under ISIP Programme, Spain, IDI-20130304 APTAFOOD.From the European Union’s Seventh Framework Programme managed by REA – Research Executive Agency (FP7/2007-2013) under grant agreement Nos. 265409 μAQUA, 315285 CIGUATOOLS and 312184 PHARMASEA. Araceli Tobío Ageitos is supported by a fellowship from Fundación Juana de Vega, Spain

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© 2014 The Authors. Published by Elsevier Inc. This article is available under the Creative Commons CC-BY-NC-ND license
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