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Title: Diva/BclB regulates differentiation by inhibiting NDPKB/Nm23H2-mediated neuronal differentiation in PC-12 cells
Authors: Lim, J.Q.R
Lu, J 
He, B.P 
Keywords: bclb protein
nucleoside diphosphate kinase NM23
protein bcl 2
unclassified drug
animal cell
cell cycle arrest
cell cycle S phase
cell nucleus
cell structure
controlled study
gene overexpression
nerve cell differentiation
nerve fiber growth
nuclear localization signal
PC12 cell
protein expression
protein function
Cell Cycle
Cell Differentiation
Gene Expression Regulation
NM23 Nucleoside Diphosphate Kinases
Nucleoside-Diphosphate Kinase
PC12 Cells
Protein Transport
Proto-Oncogene Proteins c-bcl-2
Signal Transduction
Issue Date: 2012
Publisher: BioMed Central Ltd.
Citation: Lim, J.Q.R, Lu, J, He, B.P (2012). Diva/BclB regulates differentiation by inhibiting NDPKB/Nm23H2-mediated neuronal differentiation in PC-12 cells. BMC Neuroscience 13 (1) : 123. ScholarBank@NUS Repository.
Abstract: Background: Diva (death inducer binding to vBcl-2 and Apaf-1)/BclB is a Bcl-2 family member, which is known for its function in apoptosis. Diva/BclB has been shown to interact with NDPKB/Nm23H2, which is involved in cellular differentiation. Thus far, there has been no direct evidence of Diva/BclB having a role in differentiation. In the present study, we investigated the expression of Diva/BclB and NDPKB/Nm23H2 during differentiation in PC-12 cell line.Results: Our results show that after differentiation, Diva/BclB expression was decreased and reciprocally, NDPKB/Nm23H2 expression was increased and it translocated into the nucleus. Overexpression of NDPKB/Nm23H2 promoted PC-12 neuronal differentiation by increasing neurite outgrowth and arresting cell cycle progression. There was a concurrent downregulation of Diva/Boo when NDPKB/Nm23H2 was overexpressed, which mirrors the effect of NGF on PC-12 cell differentiation. Overexpression of Diva/BclB did not change the expression level of NDPKB/Nm23H2, but inhibited its nuclear localization. Cells that overexpressed Diva/BclB presented a decreased percentage of differentiated cells and average neurite length was shortened. This was due to an increase in the formation of Diva/BclB and NDPKB/Nm23H2 complexes as well as Diva/BclB and β-tubulin complexes. Concomitantly, there was a decrease in formation of NDPKB/Nm23H2 and β-tubulin complexes. Overexpression of Diva/BclB also resulted in a higher percentage of S-phase cells.Conclusion: Our results showed a novel role for Diva/BclB in neuronal differentiation. Its downregulation during neuronal differentiation may be necessary to allow NDPKB/Nm23H2 and β-tubulin interaction that promotes NDPKB/Nm23H2 mediated differentiation. © 2012 Lim et al.; licensee BioMed Central Ltd.
Source Title: BMC Neuroscience
ISSN: 14712202
DOI: 10.1186/1471-2202-13-123
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