A Novel Tumor Suppressor Cylindromatosis

Abstract: The familial cylindromatosis (CYLD) tumor suppressor has been identified as a novel cytokine which has the activity of deubiquitinating enzyme. It is known that TNF-receptor-associated factor 2 (TRAF2) can be connected to poly ubiquitin chains linked through either lysine 48 or lysine 63， the former leads to its degradation and the latter seems to lead to the assembly of IKK kinase (TAB1/TAB2/TAK1) that activates IKK， and finally activates NF-κB. The likely model is that CYLD functions to turn TNF-receptor signaling off by removing lysine-63-linked poly ubiquitin chains from TRAF2， which acts as a negative regulator of NF-κB signalling pathway. CYLD dysfunction may result in excessive activation of NF-κB and leads to many pathological and physiological reactions. Therefore simple pharmacological agents like sodium salicylate and prostaglandin A1 suggests a strategy to restore normal growth control in patients suffering from familial cylindromatosis

CSTR: 32200.14.cjcb.2004.06.0011