Inducible and constitutive transcription factors in the mammalian nervous system: control of gene expression by Jun, Fos and Krox, and CREB/ATF proteins
Identifieur interne : 000C32 ( Main/Exploration ); précédent : 000C31; suivant : 000C33Inducible and constitutive transcription factors in the mammalian nervous system: control of gene expression by Jun, Fos and Krox, and CREB/ATF proteins
Auteurs : T. Herdegen [Allemagne] ; J. D. Leah [Australie]Source :
- Brain Research Reviews [ 0165-0173 ] ; 1998.
Abstract
This article reviews findings up to the end of 1997 about the inducible transcription factors (ITFs) c-Jun, JunB, JunD, c-Fos, FosB, Fra-1, Fra-2, Krox-20 (Egr-2) and Krox-24 (NGFI-A, Egr-1, Zif268); and the constitutive transcription factors (CTFs) CREB, CREM, ATF-2 and SRF as they pertain to gene expression in the mammalian nervous system. In the first part we consider basic facts about the expression and activity of these transcription factors: the organization of the encoding genes and their promoters, the second messenger cascades converging on their regulatory promoter sites, the control of their transcription, the binding to dimeric partners and to specific DNA sequences, their trans-activation potential, and their posttranslational modifications. In the second part we describe the expression and possible roles of these transcription factors in neural tissue: in the quiescent brain, during pre- and postnatal development, following sensory stimulation, nerve transection (axotomy), neurodegeneration and apoptosis, hypoxia–ischemia, generalized and limbic seizures, long-term potentiation and learning, drug dependence and withdrawal, and following stimulation by neurotransmitters, hormones and neurotrophins. We also describe their expression and possible roles in glial cells. Finally, we discuss the relevance of their expression for nervous system functioning under normal and patho-physiological conditions.
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DOI: 10.1016/S0165-0173(98)00018-6
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Leah</name><affiliation wicri:level="1"><country xml:lang="fr">Australie</country><wicri:regionArea>School of Biomedical Sciences, Griffith University, 4111 Nathan</wicri:regionArea><wicri:noRegion>4111 Nathan</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Brain Research Reviews</title><title level="j" type="abbrev">BRESR</title><idno type="ISSN">0165-0173</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1998">1998</date><biblScope unit="volume">28</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="370">370</biblScope><biblScope unit="page" to="490">490</biblScope></imprint><idno type="ISSN">0165-0173</idno></series><idno type="istex">50FA6689CCD0DF2FC37D1A20990311DAA0F92D32</idno><idno type="DOI">10.1016/S0165-0173(98)00018-6</idno><idno type="PII">S0165-0173(98)00018-6</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0165-0173</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">This article reviews findings up to the end of 1997 about the inducible transcription factors (ITFs) c-Jun, JunB, JunD, c-Fos, FosB, Fra-1, Fra-2, Krox-20 (Egr-2) and Krox-24 (NGFI-A, Egr-1, Zif268); and the constitutive transcription factors (CTFs) CREB, CREM, ATF-2 and SRF as they pertain to gene expression in the mammalian nervous system. In the first part we consider basic facts about the expression and activity of these transcription factors: the organization of the encoding genes and their promoters, the second messenger cascades converging on their regulatory promoter sites, the control of their transcription, the binding to dimeric partners and to specific DNA sequences, their trans-activation potential, and their posttranslational modifications. In the second part we describe the expression and possible roles of these transcription factors in neural tissue: in the quiescent brain, during pre- and postnatal development, following sensory stimulation, nerve transection (axotomy), neurodegeneration and apoptosis, hypoxia–ischemia, generalized and limbic seizures, long-term potentiation and learning, drug dependence and withdrawal, and following stimulation by neurotransmitters, hormones and neurotrophins. We also describe their expression and possible roles in glial cells. Finally, we discuss the relevance of their expression for nervous system functioning under normal and patho-physiological conditions.</div></front></TEI><affiliations><list><country><li>Allemagne</li><li>Australie</li></country><region><li>Schleswig-Holstein</li></region><settlement><li>Kiel</li></settlement></list><tree><country name="Allemagne"><region name="Schleswig-Holstein"><name sortKey="Herdegen, T" sort="Herdegen, T" uniqKey="Herdegen T" first="T." last="Herdegen">T. Herdegen</name></region></country><country name="Australie"><noRegion><name sortKey="Leah, J D" sort="Leah, J D" uniqKey="Leah J" first="J. D." last="Leah">J. D. Leah</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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