摘要
Thec-JunN-terminalkinases(JNKs)areclassicstress-activatedproteinkinases.ManycellularstresseshavebeenshowntostimulateJNKactivation.Inthisreview,wefocusonribotoxicstressesbasedontheirmultiplebiologicalpotenciesincludinganti-HIV-1activity.Someofthefunctionsofribotoxinsandthesignalingtransductionpathwaythatmediatedarementioned.Differentfromotherstimulators,ribotoxicstressesactonspecialmotifsof28SrRNAintranslationallyactivemammalribosomes.BindinganddamagingonthemotifleadstoJNKactivationandsubsequentlybiologicalresponsetothesignalinitiator,whichisnamedribotoxicstressresponse.
出版日期
2005年06月16日(中国期刊网平台首次上网日期,不代表论文的发表时间)