Abstract
AbstractThe tumor suppressor p53 has been shown to be essential in apoptosis induced by irradiation, deregulated c‐Myc expression and anti‐cancer drugs. The protein level of p53 was moderately increased when the B cell line WEHI‐231 undergoes apoptosis by B cell receptor (BCR) crosslinking. However, overexpression of a dominant negative form of p53, p53DD, abolished DNA binding activity of p53 almost completely but failed to block BCR‐mediated death of WEHI‐231, suggesting that p53‐mediated transactivation is not required for BCR‐mediated apoptosis of WEHI‐231. Moreover, B cells of p53‐deficient mice underwent cell death upon BCR crosslinking as efficiently as those of normal littermates, indicating that p53 is not essential for BCR‐mediated apoptosis of normal B cells. Although a previous report suggested that p53 is required for BCR‐mediated apoptosis through its transactivation, our data strongly argue that p53 is not required for BCR‐mediated apoptosis.
Published Version
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