cIAP2 disfunction was implicated in mucosa-associated lymphoid tissue (MALT) lymphomas

10-03-2006

According to a study from the United States, "The pathogenesis of MALT lymphomas is associated with independent chromosomal translocations that lead to the upregulation of either BCL10 or MALT1 or the generation of a fusion protein, cIAP2-MALT1. While both BCL10 and MALT1 are critically involved in antigen receptor-mediated NF-kappa B activation, the role of cIAP2 is not clear."

"Here we show that cIAP2 is a ubiquitin ligase (E3) of BCL10 and targets it for degradation, inhibiting antigen receptor-mediated cytokine production. cIAP2-MALT1 lacks E3 activity, and concomitantly, the BCL10 protein is stabilized in MALT lymphomas harboring this fusion. Furthermore, BCL10 and cIAP2-MALT1 synergistically activate NF-kappa B," explained S.M. Hu and colleagues, University of Pennsylvania.

The researchers concluded, "These results reveal cIAP2 as an inhibitor of antigenic signaling and implicate its disfunction in MALT lymphomas."

Hu and colleagues published the results of their research in the Journal of Clinical Investigation (cIAP2 is a ubiquitin protein ligase for BCL10 and is dysregulated in mucosa-associated lymphoid tissue lymphomas. J Clin Invest, 2006;116(1):174-181).

For additional information, contact X.L. Yang, University of Pennsylvania, 421 Curie Blvd., Room 610, Philadelphia, PA 19104, USA.