B-cell specific activator protein

F14. Foss, H. D., Reusch, R., Demel, G., Lenz, G., Anagnostopoulos, I., Hummel, M., and Stein, H., Frequent expression of the B-cell-specific activator protein in Reed-Sternberg cells of classical Hodgkin s disease provides further evidence for its B-cell origin. Blood 94,3108-3113 (1999). 

K28. Krenacs, L., Himmelmann, A. W., Quintanilla-Martinez, L., Fest, T., Riva, A., Wellmann, A., Bagdi, E., Kehrl, J. H., Jaffe, E. S., and Raffeld, M., Transcription factor B-cell-specific activator protein (BSAP) is differentially expressed in B cells and in subsets of B-cell lymphomas. Blood 92, 1308-1316(1998). 

Krenacs L, Himmelmann AW, Quintanilla-Martinez L, et al. Transcription factor B cell specific activator protein is differentially expressed in B cells and in subsets of B cell lymphomas. Blood. 1998 92 1308-1316. 

PAX-5, a B-cell specific activation protein, is commonly expressed in these tumors. 

Dong HY, Liu W, Cohen P, et al. B-cell specific activation protein encoded by the PAX-5 gene is commonly expressed in Merkel cell carcinoma and small cell carcinomas. Am J Surg Pathol. 2005 29 687-692. 

In line with expression of A3 adenosine receptors in cells and tissues like mast cells, spleen and thymus putative binding sites for a number of transcription factors relevant for protein expression in inflammation and infection were identified in the promoter region of the A3 receptor gene (Atkinson et al. 1997 Zhao et al. 1999). These include activator protein 1 (AP-1) which regulates gene expression in response to viral and bacterial infections or to stimulation by cytokines. Additional binding sites for transcription factors with specificity for immune cells are for the T cell-specific T cell factor F-2-a (TcF-2-a) and for the B cell-specific E2aECB. 

Many inflammatory cytokines including IL-8 are regulated at transcriptional levels, and a variety of transcription factors such as nuclear factor-K B (NFkB) and activator protein-1 (AP-1) play important roles in such processes. Abe and coworkers [71] demonstrated that CAM repressed TNF-a-induced AP-1 activation in human bronchial epithelial cells. We studied the effect of EM and CAM on the phorbol myristate acetate (PMA)-induced activation of NFkB and AP-1. Pretreatment of EM and CAM before the PMA treatment showed an inhibitory effect on both of the transcription factors as assessed by electrophoretic mobility shift assay (EMSA) (Fig. 14) [20]. In contrast, the macrolides showed no effect on the activation of cyclic AMP-responsive element binding protein (CREB), suggesting that the suppressive effect on some transcription factors is specific. We further evaluated the effect of EM on the phosphorylation of inhibitor of NFkB (IkB), which is a crucial step for transactivation of NFkB. EM did not influence the phosphorylation processes in vitro (Okazaki et at, unpublished data, January 2001). These data suggest that EM acts at the process of nuclear translocation of... 

Herrscher, R. F., Kaplan, M. H., Lelsz, D. L., Das, C., Scheurmann, R., and Tucker, P. W, (1995). The immunoglobulin heavy-chain matrix-associating regions are bound by Bright A B cell-specific rrans-activator that describes a new DNA-binding protein family. Genes Dev. 9, 3067-3082. 

The specific role of vitamin A in tissue differentiation has been an active area of research. The current thinking, developed in 1979, involves initial dehvery of retinol by holo-B >V (retinol-binding protein) to the cell cytosol (66). Retinol is then ultimately oxidized to retinoic acid and binds to a specific cellular retinoid-binding protein and is transported to the nucleus. Retinoic acid is then transferred to a nuclear retinoic acid receptor (RAR), which enhances the expression of a specific region of the genome. Transcription occurs and new proteins appear during the retinoic acid-induced differentiation of cells (56). 

Associated with NA depletion from host nuclei was the diminution and deformation of these nuclei, significant depletion of host nucleoskeletal protein lamin b, and significant reductions in levels of host cell RNA, protein and acid phosphatase activity. In contrast, host infiltrating cells showed no such changes, supporting an infected cell-specific effect. These observations support the possibility that NA are synthesized by the parasite and modulate host nuclear functions. However, release of other parasite secretory products, not analysed, might have been inhibited in these experiments also. 

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