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Upregulation of MDM2-like p53 binding protein (arrow) following adenovirus-based TNFaRp55 gene transfer into rheumatoid synovial fibroblasts. (Analysis performed by Elena Neumann, University of Regensburg, Germany, using a Clontech Atlas® DNA array system. TNFaRp55 Ad5 generously provided by Dr John Mountz, University of Birmingham, AL, USA.)
- For example, overexpression of tumour necrosis factor-α receptor p55 in RA synovial fibroblasts using adenovirus-based gene therapy results in upregulation of a MDM2-like p53-binding protein (Fig. 1), which is presumably involved in regulation and cellular distribution of various members of the p53 family [13,14,34,35].