Fuse binding protein antagonizes the transcription activity of @entity5 suppressor protein XXXX .

@entity1 @entity96 @entity5 @entity13676 @entity3544 @entity24154 @entity876 @entity71799
BACKGROUND: @entity24154 ( @entity24154 ) is a transactivator of transcription of @entity1 c-myc proto-oncogene and expressed mainly in undifferentiated cells. It is also present in differentiated normal cells albeit with very low background. @entity24154 is abundantly expressed in the majority of @entity96 and has been implicated in @entity5 development. Although it down-regulates the expression of proapoptotic @entity3544 protein, it is not known whether @entity24154 also interacts and antagonizes the function of @entity5 suppressor protein @entity876 . METHODS: Western blotting was carried out to detect the expression level of @entity24154 , @entity3544 and @entity876 , and also @entity876 regulatory factors, @entity71799 and @entity13676 ; real-time quantitative PCR was done to determine the fold change in mRNA levels of target proteins; immunoprecipitation was carried out to determine the interaction of @entity24154 with @entity876 , @entity71799 and @entity13676 . Cells stably knockdown for either @entity24154 ; @entity876 or @entity71799 were examined for @entity876 reporter activity under normal and radiation-induced stress. RESULTS: @entity24154 physically interacted with @entity876 , impairing its transcription activity and reducing @entity876 -mediated sensitivity to cellular stress. Knockdown of @entity24154 expression activated @entity876 -mediated response to cellular stress while transient expression of @entity24154 in @entity24154 -knockdown cells restored the inhibition of @entity876 activity. @entity24154 not only interacted with both @entity71799 and @entity13676 , which, respectively, function as positive and negative regulators of @entity876 , but also regulated their expression under cellular stress. In @entity24154 knockdown cells, @entity13676 expression was down-regulated under radiation-induced stress whereas expression of @entity71799 and @entity3544 were significantly up-regulated suggesting @entity24154 as a potential regulator of these proteins. We hypothesize that the @entity24154 -mediated suppression of @entity876 activity may occur via preventing the interaction of @entity876 with @entity71799 as well as by @entity24154 -mediated regulation of @entity876 regulatory proteins, @entity13676 and @entity71799 . Since @entity24154 suppresses @entity876 activity and is overexpressed in most @entity5 , it may have a possible role in tumorigenesis. CONCLUSION: @entity24154 physically interacts with @entity876 , functions as a regulator of @entity876 -regulatory proteins ( @entity13676 and @entity71799 ), and suppresses @entity876 transactivation activity under radiation-induced cellular stress. Since it is abundantly expressed in most @entity5 , it may have implication in tumorigenesis and thus may be a possible target for drug development.
