Involvement of NAK‐1, the human nur77 homologue, in surface IgM‐mediated apoptosis in Burkitt lymphoma cell line BL41

Publisher Website
Google Scholar
Abstract
The induction of apoptosis via surface IgM (sIgM) in immature B cells requires de novo transcription. To investigate the regulation of activation‐induced cell death (AICD) in B cells we used a cell line model consisting of an Epstein‐Barr virus‐negative Burkitt lymphoma cell line (BL41), which is highly sensitive, and a subclone which is resistant to sIgM‐mediated apoptosis (BL41/B5). Resistance in this cell line was not due to down‐regulation of sIgM or functional impairment in signal transduction of the surface Ig complex. The zinc finger transcription factor nur77 has been implicated to play an important role in CD3‐mediated apoptosis in murine T cells. We were able to demonstrate that surface IgM ligation and subsequent apoptosis in BL41 cells is associated with a concomitant induction of NAK‐1, the human nur77 homologue. Induction of NAK‐1 mRNA and DNA binding activity in the nucleus could be readily observed by means of Northern blot and electrophoretic mobility shift assay, respectively. In contrast, the resistant clone BL41/B5 did not show any NAK‐1 expression upon stimulation. This suggests a role for NAK‐1 in sIgM‐mediated apoptosis of immature B cells.