TAILIEUCHUNG - Báo cáo khoa học: The calcium-binding domain of the stress protein SEP53 is required for survival in response to deoxycholic acid-mediated injury

Stress protein responses have evolved in part as a mechanism to protect cells from the toxic effects of environmental damaging agents. Oesophageal squamous epithelial cells have evolved an atypical stress response that results in the synthesis of a 53 kDa protein of undefined function named squamous epithelial-induced stress protein of 53 kDa (SEP53). | iFEBS Journal The calcium-binding domain of the stress protein SEP53 is required for survival in response to deoxycholic acid-mediated injury Joanne Darragh1 z Mairi Hunter1 Elizabeth Pohler2 Lenny Nelson2 John F. Dillon1 Rudolf Nenutil3 Borek Vojtesek3 Peter E. Ross1 Neil Kernohan1 and Ted R. Hupp2 1 Division of Pathology and Neurosciences University of Dundee UK 2 University of Edinburgh Cancer Centre CRUK Cellsignalling Unit UK 3 Masaryk MemorialCancer Institute BRNO Czech Republic Keywords Barrett s apoptosis calcium deoxycholic acid SEP53 stress response Correspondence T. R. Hupp University of Edinburgh Cancer Centre CRUK Cell Signalling Unit South Crewe Road Edinburgh EH4 2XR UK E-mail Present address MRC Protein Phosphorylation Unit University of Dundee UK Received 12 December 2005 revised 2 February 2006 accepted 28 February 2006 doi Stress protein responses have evolved in part as a mechanism to protect cells from the toxic effects of environmental damaging agents. Oesophageal squamous epithelial cells have evolved an atypical stress response that results in the synthesis of a 53 kDa protein of undefined function named squamous epithelial-induced stress protein of 53 kDa SEP53 . Given the role of deoxycholic acid DCA as a potential damaging agent in squamous epithelium we developed assays measuring the effects of DCA on SEP53-mediated responses to damage. To achieve this we cloned the human SEP53 gene developed a panel of monoclonal antibodies to the protein and showed that SEP53 expression is predominantly confined to squamous epithelium. Clonogenic assays were used to show that SEP53 can function as a survival factor in mammalian cell lines can attenuate DCA-induced apoptotic cell death and can attenuate DCA-mediated increases in intracellular free calcium. Deletion of the highly conserved EF-hand calcium-binding domain in SEP53 neutralizes the colony survival activity of the protein neutralizes the .

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