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Báo cáo khoa học: " Differential protection by wildtype vs. organelle-specific Bcl-2 suggests a combined requirement of both the ER and mitochondria in ceramide-mediated caspase-independent programmed cell death"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Radiation Oncology cung cấp cho các bạn kiến thức về ngành y đề tài: " Differential protection by wildtype vs. organelle-specific Bcl-2 suggests a combined requirement of both the ER and mitochondria in ceramide-mediated caspase-independent programmed cell death. | Radiation Oncology BioMed Central Research Differential protection by wildtype vs. organelle-specific Bcl-2 suggests a combined requirement of both the ER and mitochondria in ceramide-mediated caspase-independent programmed cell death Andrea Deerberg1 Justyna Sosna1 Lutz Thon1 Claus Belka2 and Dieter Adam 1 Open Access Address Institut fur Immunologie Christian-Albrechts-Universitat Kiel 24105 Kiel Germany and 2Klinik und Poliklinik fur Strahlentherapie und Radioonkologie Ludwig-Maximilians Universitat Munchen 81377 Munchen Germany Email Andrea Deerberg - Jung@imm.uni-luebeck.de Justyna Sosna - pumpard@yahoo.com Lutz Thon - lutz-thon@web.de Claus Belka - claus.belka@med.uni-muenchen.de Dieter Adam - dadam@email.uni-kiel.de Corresponding author Published 9 October 2009 Received 22 August 2009 Radiation Oncology 2009 4 41 doi 10.1186 1748-717X-4-41 Accepted 9 October 2009 This article is available from http www.ro-journal.cOm content 4 1 41 2009 Deerberg et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http creativecommons.org licenses by 2.0 which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background Programmed cell death PCD is essential for development and homeostasis of multicellular organisms and can occur by caspase-dependent apoptosis or alternatively by caspaseindependent PCD ciPCD . Bcl-2 a central regulator of apoptosis localizes to both mitochondria and the endoplasmic reticulum ER . Whereas a function of mitochondrial and ER-specific Bcl-2 in apoptosis has been established in multiple studies corresponding data for ciPCD do not exist. Methods We utilized Bcl-2 constructs specifically localizing to mitochondria Bcl-2 ActA the ER Bcl-2 cb5 both Bcl-2 WT or the cytosol nucleus Bcl-2 ATM and determined their protective effect on ceramide-mediated ciPCD in transiently and stably transfected .