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Molecular and Cellular Biology, July 2009, p. 3633-3643, Vol. 29, No. 13
0270-7306/09/$08.00+0 doi:10.1128/MCB.00362-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

School of Medicine, Department of Biological Sciences and Biotechnology, State Key Laboratory of Biomembrane and Membrane Biotechnology, Tsinghua University, Beijing, China,1 Northwest Plateau Institute of Biology, Chinese Academy of Sciences, Xining, and Graduate University of Chinese Academy of Sciences, Beijing, China,2 College of Life Science, Beijing Normal University, Beijing, China3
Received 20 March 2009/ Accepted 20 April 2009
Neuronal differentiation is tightly regulated by a variety of factors. In a search for neuron-specific genes, we identified a highly conserved novel zinc finger protein, ZNF536. We observed that ZNF536 is most abundant in the brain and, in particular, is expressed in the developing central nervous system and dorsal root ganglia and localized in the cerebral cortex, hippocampus, and hypothalamic area. During neuronal differentiation of P19 cells induced by retinoic acid (RA), ZNF536 expression is increased at an early stage, and it is maintained at a constant level in later stages. Overexpression of ZNF536 results in an inhibition of RA-induced neuronal differentiation, while depletion or mutation of the ZNF536 gene results in an enhancement of differentiation. We further demonstrated that ZNF536 inhibits expression of neuron-specific marker genes, possibly through the inhibition of RA response element-mediated transcriptional activity, as overexpression of RA receptor
can rescue the inhibitory role of ZNF536 in neuronal differentiation and neuron-specific gene expression. Our studies have identified a novel zinc finger protein that negatively regulates neuron differentiation.
Published ahead of print on 27 April 2009.
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