The effect of C-terminal fragment of JNK2 on the stability of p53 and cell proliferation

查看全文 作　　者：[1]ZhiMinYIN;[1]JianSIMA;[1]YiFanWU;[1]JianZHU;[2]YongJIANG

机构地区：[1]JiangsuProvinceKeyLaboratoryofBiochemistryandMolecularBiology,CollegeofLifeScience,NanjingNormalUniversity,Nanjing210097,China;[2]DepartmentofPathophysiologyandKeyLabforShockandMicrocirculationofPLA,TheFirstMilitaryMedicalUniversity,Guangzhou510515,China

出　　处：《Cell Research》索引2004年第14卷第5期,共5页

基　　金：supported by National Natural Science Foundation of China(No.30270556);The National Basic Research Program(No.2002CB513004). 摘　　要：The basal activity of JNK is low in normal growing cells and inactivated JNK targets p53 for ubiquitination. To elucidate if the C-terminal part of JNK is responsible for its binding to p53, the low background tet-off inducible NIH3T3 cell line was selected by luciferase reporter gene and a double stable C-JNK Aa (203-424) cell line was established. After withdrawing tetracycline, the C-JNK fragment expression was induced and cell growth was dramati- cally inhibited 24 h later. However, the expresion of p53 was found to be increased after the induction of C-JNK fragment, evaluated by transfecting p21waf-luciferase reporter genes. Our further studies showed that C-JNK fragment could form complex with p53 both in vivo and in vitro. Induction of C-JNK fragment in vivo can increase p53 stability by inhibiting p53 ubiquitination. 关键词：增殖细胞有丝分裂原活化蛋白激酶表达信号转导

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The effect of C-terminal fragment of JNK2 on the stability of p53 and cell proliferation

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