Abstract
Abstract LMP1 is an Epstein-Barr virus encoded protein that is expressed on the surface of latently infected cells and is known to promote cell survival through activation of the NFκB pathway. Previously our lab developed an immortalized B cell line from a patient with non-X-linked HIGM in which LMP1 is conditionally expressed under the control of a tetracycline-inducible promoter (pt1-LCLtet cells). Analysis of these cells revealed an increased level of apoptosis even in the continuous presence of LMP1 stimulation. In addition, analysis of NFκB/Rel subunits showed a markedly lower expression of c-Rel (c-Rel75) and the presence of a novel 25 kD form (c-Rel25) in pt1but not control-LCLtetcells. Western analysis of immunoprecipitated c-Rel revealed several higher mw forms in pt1- vs. control-LCLtet cells. To investigate the phosphorylation status of c-Rel75 in the pt1-LCLtet cells, in-vivo labeling was carried out and immunoprecipitation of extracts with anti-c-Rel antibodies revealed that c-Rel75 is hyperphosphorylated in these cells. Therefore, we hypothesize that hyperphosphorylation of c-Rel75 targets a post-translational processing event that results in both the reduced level of c-Rel75 and the appearance of the 25 kD form observed in pt1-LCLtet cells. Importantly, the low abundance of c-Rel75 appears to be closely linked to ongoing apoptosis which is not inhibited by LMP1 signaling. (Supported by AI37081)
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