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Papers In Press, published online ahead of print May 31, 2001
School of Biomedical Sciences, University of Nottingham, Nottingham NG7 2UH
Corresponding Author: peter.shaw{at}nottingham.ac.uk
Apoptosis involves the cessation of cellular processes, the breakdown of intracellular organelles and, finally, the non-phlogistic clearance of apoptotic cells from the body. Important for these events is a family of proteases, caspases, which are activated by a proteolytic cleavage cascade and drive apoptosis by targeting key proteins within the cell. Here, we demonstrate that SRF, a transcription factor essential for proliferative gene expression, is cleaved by caspases, that this cleavage occurs in proliferating murine fibroblasts and can be induced in the human B-cell line BJAB. We identify the two major sites at which SRF cleavage occurs as D245 and D254, the caspases responsible for the cleavage and generate a mutant of SRF resistant to cleavage in BJAB cells. Investigation of the physiological and functional significance of SRF cleavage reveals that it correlates with the loss of c-fos expression, whereby neither SRF cleavage fragment retains transcriptional activity. Moreover, the expression of a non-cleavable SRF in BJAB cells suppresses apoptosis induced by Fas crosslinking. These results suggest that for apoptosis to proceed, the transcriptional events promoting cell survival and proliferation, in which SRF is involved, must first be inactivated.
J. Biol. Chem, 10.1074/jbc.M103877200
Submitted on May 1, 2001
Revised on May 31, 2001
Accepted on May 31, 2001
Serum response factor (SRF) cleavage by caspases 3 and 7 linked to apoptosis in human BJAB cells
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