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Consolidation of transient ionotropic glutamate signals through nuclear transcription factors in the brain

Identifieur interne : 000A47 ( Main/Exploration ); précédent : 000A46; suivant : 000A48

Consolidation 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 :

RBID : ISTEX:48DD146874C32F6299C83F2ABBB815D3A3289167

English descriptors

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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Le document en format XML

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