Consolidation of transient ionotropic glutamate signals through nuclear transcription factors in the brain
Identifieur interne : 000A28 ( Main/Exploration ); précédent : 000A27; suivant : 000A29Consolidation of transient ionotropic glutamate signals through nuclear transcription factors in the brain
Auteurs : Yukio Yoneda [Japon] ; Nobuyuki Kuramoto [Japon] ; Tomoya Kitayama [Japon] ; Eiichi Hinoi [Japon]Source :
- Progress in Neurobiology [ 0301-0082 ] ; 2000.
English descriptors
- KwdEn :
- AMPA, dl-α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid, AP1, activator protein-1, BDNF, brain derived neurotrophic factor, CRE, cyclic AMP response element, CREB, cyclic AMP response element binding protein, GC, glucocorticoid, GRE, glucocorticoid response element, GREB, glucocorticoid response element binding protein, Glu, glutamic acid, Gly, glycine, HSP, heat shock protein, IEG, immediate early gene, KA, kainic acid, MK-801, (+)5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine, NGF, nerve growth factor, NMDA, N-methyl-d-aspartic acid, NaF, sodium fluoride, NaGP, sodium β-glycerophosphate, PCR, polymerase chain reaction, RT, reverse transcription, SRE, serum response element, TPA, 12-O-tetradecanoylphorbol 13-acetate, TRE, 12-O-tetradecanoylphorbol 13-acetate response element.
Abstract
Long-lasting alterations of neuronal functions could involve mechanisms associated with consolidation of transient extracellular signals through modulation of de novo synthesis of particular functional proteins in the brain. In eukaryotes, protein de novo synthesis is mainly under the control at the level of gene transcription by transcription factors in the cell nucleus. Transcription factors are nuclear proteins with an ability to recognize particular core nucleotides at the upstream and/or downstream of target genes, and thereby to modulate the activity of RNA polymerase II that is responsible for the formation of mRNA from double stranded DNA. Gel retardation electrophoresis is widely employed for conventional detection of DNA binding activities of a variety of transcription factors with different protein motifs. Extracellular ionotropic glutamate (Glu) signals lead to rapid and selective potentiation of DNA binding of the nuclear transcription factor activator protein-1 (AP1) that is a homo- and heterodimeric complex between Jun and Fos family members, in addition to inducing expression of the corresponding proteins, in a manner unique to each Glu signal in murine hippocampus. Therefore, extracellular Glu signals may be differentially transduced into the nucleus to express AP1 with different assemblies between Jun and Fos family members, and thereby to modulate de novo synthesis of the individual target proteins at the level of gene transcription in the hippocampus. Such mechanisms may be operative on synaptic plasticity as well as delayed neuronal death through consolidation of alterations of a variety of cellular functions induced by transient extracellular signals in the brain.
Url:
DOI: 10.1016/S0301-0082(00)00036-8
Affiliations:
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(+)5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine</term><term>NGF, nerve growth factor</term><term>NMDA, N-methyl-d-aspartic acid</term><term>NaF, sodium fluoride</term><term>NaGP, sodium β-glycerophosphate</term><term>PCR, polymerase chain reaction</term><term>RT, reverse transcription</term><term>SRE, serum response element</term><term>TPA, 12-O-tetradecanoylphorbol 13-acetate</term><term>TRE, 12-O-tetradecanoylphorbol 13-acetate response element</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Long-lasting alterations of neuronal functions could involve mechanisms associated with consolidation of transient extracellular signals through modulation of de novo synthesis of particular functional proteins in the brain. In eukaryotes, protein de novo synthesis is mainly under the control at the level of gene transcription by transcription factors in the cell nucleus. Transcription factors are nuclear proteins with an ability to recognize particular core nucleotides at the upstream and/or downstream of target genes, and thereby to modulate the activity of RNA polymerase II that is responsible for the formation of mRNA from double stranded DNA. Gel retardation electrophoresis is widely employed for conventional detection of DNA binding activities of a variety of transcription factors with different protein motifs. Extracellular ionotropic glutamate (Glu) signals lead to rapid and selective potentiation of DNA binding of the nuclear transcription factor activator protein-1 (AP1) that is a homo- and heterodimeric complex between Jun and Fos family members, in addition to inducing expression of the corresponding proteins, in a manner unique to each Glu signal in murine hippocampus. Therefore, extracellular Glu signals may be differentially transduced into the nucleus to express AP1 with different assemblies between Jun and Fos family members, and thereby to modulate de novo synthesis of the individual target proteins at the level of gene transcription in the hippocampus. Such mechanisms may be operative on synaptic plasticity as well as delayed neuronal death through consolidation of alterations of a variety of cellular functions induced by transient extracellular signals in the brain.</div></front></TEI><affiliations><list><country><li>Japon</li></country></list><tree><country name="Japon"><noRegion><name sortKey="Yoneda, Yukio" sort="Yoneda, Yukio" uniqKey="Yoneda Y" first="Yukio" last="Yoneda">Yukio Yoneda</name></noRegion><name sortKey="Hinoi, Eiichi" sort="Hinoi, Eiichi" uniqKey="Hinoi E" first="Eiichi" last="Hinoi">Eiichi Hinoi</name><name sortKey="Kitayama, Tomoya" sort="Kitayama, Tomoya" uniqKey="Kitayama T" first="Tomoya" last="Kitayama">Tomoya Kitayama</name><name sortKey="Kuramoto, Nobuyuki" sort="Kuramoto, Nobuyuki" uniqKey="Kuramoto N" first="Nobuyuki" last="Kuramoto">Nobuyuki Kuramoto</name><name sortKey="Yoneda, Yukio" sort="Yoneda, Yukio" uniqKey="Yoneda Y" first="Yukio" last="Yoneda">Yukio Yoneda</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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