title: The effect of C-terminal fragment of JNK2 on the stability of p53 and cell proliferation.
abstract: 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 dramatically inhibited 24 h later. However, the expression 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.
authors.affiliation: Jiangsu Province Key Laboratory of Biochemistry and Molecular Biology, College of Life Science, Nanjing Normal University, Nanjing 210097, China. Zhiminy_2000@yahoo.com
authors.forename: Zhi Min
authors.initials: ZM
authors.lastname: Yin
authors.forename: Jian
authors.initials: J
authors.lastname: Sima
authors.forename: Yi Fan
authors.initials: YF
authors.lastname: Wu
authors.forename: Jian
authors.initials: J
authors.lastname: Zhu
authors.forename: Yong
authors.initials: Y
authors.lastname: Jiang
mesh_terms: D016475:3T3 Cells; D000818:Animals; D002460:Cell Line; D049109:Cell Proliferation / Q000187:drug effects*; D051379:Mice; D048056:Mitogen-Activated Protein Kinase 9 / Q000737:chemistry / Q000378:metabolism*; D010446:Peptide Fragments / Q000494:pharmacology*; D013997:Time Factors; D016159:Tumor Suppressor Protein p53 / Q000187:drug effects* / Q000378:metabolism
chemical_list: D010446:Peptide Fragments; D016159:Tumor Suppressor Protein p53; D048056:Mitogen-Activated Protein Kinase 9