The Epstein-Barr virus latent membrane protein-1 (LMP1) mediates activation of NF-kappa B and cell surface phenotype via two effector regions in its carboxy-terminal cytoplasmic domain.

作者: Huen Ds , Rowe M , Croom-Carter D , Henderson Sa

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摘要: Abstract The Epstein-Barr virus (EBV) encoded latent membrane protein, LMP1, is oncogenic in rodent fibroblasts and an essential effector protein EBV-induced growth-transformation of human B lymphocytes. Previous structure-function studies with LMP1 have relied largely on fibroblast transformation as a functional readout, apparently conflicting results. We now analysed several mutants various cell types, including cells, T cells epithelial using two independent assays; (i) activation NF-kappa B, (ii) induction surface markers, CD54 CD40. results suggest that the cytosolic N-terminus not for function any type studied. third fourth transmembrane helices intracytosolic loops are dispensable but they do influence major domain appears to be C-terminus which were identified 'C-terminal activating regions', CTAR-1 (residues 194-232) CTAR-2 351-386). Whilst exact depended upon host line, was generally more important both required optimal Analysis by Rat-1 indicated many mutations poorly tolerated cells; result broad agreement published data.

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