p66SHC promotes T cell apoptosis by inducing mitochondrial dysfunction and impaired Ca2+ homeostasis

p66Shc, a redox enzyme that enhances reactive oxygen species (ROS) production by mitochondria, promotes T cell apoptosis. We have addressed the mechanisms regulating p66Shc-dependent apoptosis in T cells exposed to supraphysiological increases in [Ca 2+ ] c . p66Shc expression resulted in profound m...

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Veröffentlicht in:	Cell death and differentiation 2007-02, Vol.14 (2), p.338-347
Hauptverfasser:	Pellegrini, M, Finetti, F, Petronilli, V, Ulivieri, C, Giusti, F, Lupetti, P, Giorgio, M, Pelicci, P G, Bernardi, P, Baldari, C T
Format:	Artikel
Sprache:	eng
Schlagworte:	Adaptor Proteins, Signal Transducing - metabolism Apoptosis Apoptosis - drug effects Biochemistry Biomedical and Life Sciences Calcimycin - pharmacology Calcium - metabolism Cell Biology Cell Cycle Analysis Cell death Cytochrome Down-Regulation - drug effects Enzymes Evolutionary biology Flow Cytometry Gene Expression Regulation, Enzymologic - drug effects Homeostasis Homeostasis - drug effects Humans Jurkat Cells Kinases Life Sciences Lymphocytes Membrane Potential, Mitochondrial - drug effects Mitochondria Mitochondria - drug effects Mitochondria - enzymology Mitochondria - metabolism Oncology original-paper Oxidative stress Permeability Phosphorylation Phosphoserine - metabolism Plasma Plasma Membrane Calcium-Transporting ATPases - genetics Reactive Oxygen Species - metabolism RNA, Messenger - genetics RNA, Messenger - metabolism Shc Signaling Adaptor Proteins Src Homology 2 Domain-Containing, Transforming Protein 1 Stem Cells T-Lymphocytes - cytology T-Lymphocytes - drug effects T-Lymphocytes - immunology T-Lymphocytes - ultrastructure
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