title: Different Effects of p52SHC1 and p52SHC3 on the Cell Cycle of Neurons and Neural Stem Cells.
abstract: SHC3 is exclusively expressed in postmitotic neurons, while SHC1 is found in neural stem cells and neural precursor cells but absent in mature neurons. In this study, we discovered that suppression of p52SHC1 expression by RNA interference resulted in proliferation defects in neural stem cells, along with significantly reduced protein levels of cyclin E and cyclin A. At the same time, p52SHC3 RNAi caused cell cycle re-entry (9.54% in S phase and 5.70% in G2-M phase) in primary neurons with significantly up-regulated expression of cyclin D1, cyclin E, cyclin A, CDK2, and phosphorylated CDK2. When p52SHC3 was overexpressed, the cell cycle of neural stem cells was arrested with reduced protein levels of cyclin D1, cyclin E, and cyclin A, while overexpression of p52SHC1 did not result in significant changes in postmitotic neurons. Our results indicate that p52SHC3 plays an important role in maintaining the mitotic quiescence of neurons, while p52SHC1 regulates the proliferation of neural stem cells.
authors.affiliation: State Key Laboratory of Proteomics and, Department of Neurobiology, Institute of Basic Medical Sciences, Beijing, P. R. China.|Reproductive Medicine Center, Jinan Military General Hospital, Jinan, P. R. China.
authors.forename: Ning
authors.initials: N
authors.lastname: Tang
authors.affiliation: State Key Laboratory of Proteomics and, Department of Neurobiology, Institute of Basic Medical Sciences, Beijing, P. R. China.|Dan Lyu is currently working in Department of Pain Management, Tianjin First Center Hospital, Tianjin, P. R. China.
authors.forename: Dan
authors.initials: D
authors.lastname: Lyu
authors.affiliation: State Key Laboratory of Proteomics and, Department of Neurobiology, Institute of Basic Medical Sciences, Beijing, P. R. China.
authors.forename: Tao
authors.initials: T
authors.lastname: Liu
authors.affiliation: State Key Laboratory of Proteomics and, Department of Neurobiology, Institute of Basic Medical Sciences, Beijing, P. R. China.
authors.forename: Fangjin
authors.initials: F
authors.lastname: Chen
authors.affiliation: State Key Laboratory of Proteomics and, Department of Neurobiology, Institute of Basic Medical Sciences, Beijing, P. R. China.
authors.forename: Shuqian
authors.initials: S
authors.lastname: Jing
authors.affiliation: Reproductive Medicine Center, Jinan Military General Hospital, Jinan, P. R. China.
authors.forename: Tianyu
authors.initials: T
authors.lastname: Hao
authors.affiliation: State Key Laboratory of Proteomics and, Department of Neurobiology, Institute of Basic Medical Sciences, Beijing, P. R. China.
authors.forename: Shaojun
authors.initials: S
authors.lastname: Liu
mesh_terms: D000818:Animals; D002453:Cell Cycle / Q000502:physiology*; D002455:Cell Division / Q000502:physiology; D049109:Cell Proliferation / Q000187:drug effects; D019925:Cyclin A / Q000378:metabolism; D051357:Cyclin-Dependent Kinase 2 / Q000378:metabolism*; D058953:Neural Stem Cells / Q000378:metabolism*; D009474:Neurons / Q000378:metabolism*; D017208:Rats, Wistar; D055765:Shc Signaling Adaptor Proteins / Q000378:metabolism*; D000071425:Src Homology 2 Domain-Containing, Transforming Protein 1; D000071427:Src Homology 2 Domain-Containing, Transforming Protein 3
chemical_list: D019925:Cyclin A; D055765:Shc Signaling Adaptor Proteins; C528035:Shc1 protein, rat; C485683:Shc3 protein, rat; D000071425:Src Homology 2 Domain-Containing, Transforming Protein 1; D000071427:Src Homology 2 Domain-Containing, Transforming Protein 3; C495892:Cdk2 protein, rat; D051357:Cyclin-Dependent Kinase 2