Nucleosome assembly proteins and their interacting proteins in neuronal differentiation
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作者:
Attia, Mikael
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Inst Pasteur, Unite Genet Mol Murine, CNRS, URA 2578, F-75724 Paris 15, FranceInst Pasteur, Unite Genet Mol Murine, CNRS, URA 2578, F-75724 Paris 15, France
Attia, Mikael
[1
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Rachez, Christophe
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Inst Pasteur, Unite Regulat Epigenet, CNRS, URA 2578, F-75724 Paris 15, FranceInst Pasteur, Unite Genet Mol Murine, CNRS, URA 2578, F-75724 Paris 15, France
Rachez, Christophe
[2
]
Avner, Philip
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Inst Pasteur, Unite Genet Mol Murine, CNRS, URA 2578, F-75724 Paris 15, FranceInst Pasteur, Unite Genet Mol Murine, CNRS, URA 2578, F-75724 Paris 15, France
Avner, Philip
[1
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Rogner, Ute Christine
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Inst Pasteur, Unite Genet Mol Murine, CNRS, URA 2578, F-75724 Paris 15, FranceInst Pasteur, Unite Genet Mol Murine, CNRS, URA 2578, F-75724 Paris 15, France
Rogner, Ute Christine
[1
]
机构:
[1] Inst Pasteur, Unite Genet Mol Murine, CNRS, URA 2578, F-75724 Paris 15, France
[2] Inst Pasteur, Unite Regulat Epigenet, CNRS, URA 2578, F-75724 Paris 15, France
Neuronal differentiation from neural stem cells into mature neurons is guided by the concerted action of specific transcription factors that stepwise exercise their role in the context of defined chromatin states. Amongst the classes of proteins that influence chromatin compaction and modification are nucleosome assembly proteins (NAPs). Mammals possess several nucleosome assembly protein 1 like proteins (NAP1L) that show either ubiquitous or neuron-restricted expression. The latter group is presumably involved in the process of neuronal differentiation. Mammalian NAP1Ls can potentially form both homo- and hetero-dimers and octamers, in theory allowing thousands of different combinations to be formed. Detailed studies have been performed on several of the NAP1Ls that point to a range of molecular roles, including transcriptional regulation, nuclear import, and control of cell division. This article aims at summarizing current knowledge of the mammalian NAP1L family and its interactions. (C) 2012 Elsevier Inc. All rights reserved.