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Status: Bibliographieeintrag

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Verfasst von:Zhang, Sheng-Jia [VerfasserIn]   i
 Buchthal, Bettina [VerfasserIn]   i
 Lau, David [VerfasserIn]   i
 Hayer, Stefanie Nicole [VerfasserIn]   i
 Dick, Oliver [VerfasserIn]   i
 Schwaninger, Markus [VerfasserIn]   i
 Veltkamp, Roland [VerfasserIn]   i
 Zou, Ming [VerfasserIn]   i
 Weiss, Ursula [VerfasserIn]   i
 Bading, Hilmar [VerfasserIn]   i
Titel:A signaling cascade of nuclear calcium-CREB-ATF3 activated by synaptic NMDA receptors defines a gene repression module that protects against extrasynaptic NMDA receptor-induced neuronal cell death and ischemic brain damage
Verf.angabe:Sheng-Jia Zhang, Bettina Buchthal, David Lau, Stefanie Hayer, Oliver Dick, Markus Schwaninger, Roland Veltkamp, Ming Zou, Ursula Weiss, and Hilmar Bading
E-Jahr:2011
Jahr:March 30, 2011
Umfang:13 S.
Fussnoten:Gesehen am 16.01.2023
Titel Quelle:Enthalten in: The journal of neuroscience
Ort Quelle:Washington, DC : Soc., 1981
Jahr Quelle:2011
Band/Heft Quelle:31(2011), 13, Seite 4978-4990
ISSN Quelle:1529-2401
Abstract:Synapse-to-nucleus signaling triggered by synaptic NMDA receptors can lead to the buildup of a neuroprotective shield. Nuclear calcium activating the cAMP response element binding protein (CREB) plays a key role in neuroprotection acquired by synaptic activity. Here we show that in mouse hippocampal neurons, the transcription factor Atf3 (activating transcription factor 3) is a direct target of CREB. Induction of ATF3 expression by CREB in hippocampal neurons was initiated by calcium entry through synaptic NMDA receptors and required nuclear calcium transients and calcium/calmodulin-dependent protein kinase IV activity. Acting as a transcriptional repressor, ATF3 protects cultured hippocampal neurons from apoptosis and extrasynaptic NMDA receptor-induced cell death triggered by bath application of NMDA or oxygen-glucose deprivation. Expression of ATF3 in vivo using stereotaxic delivery of recombinant adeno-associated virus reduces brain damage following a cerebral ischemic insult in mice. Conversion of ATF3 to a transcriptional activator transforms ATF3 into a potent prodeath protein that kills neurons in cell culture and, when expressed in vivo in the hippocampus, ablates the neuronal cell layer. These results link nuclear calcium-CREB signaling to an ATF3-mediated neuroprotective gene repression program, indicating that activity-dependent shutoff of genes is an important process for survival. ATF3 supplementation may counteract age- and disease-related neuronal cell loss caused by a reduction in synaptic activity, malfunctioning of calcium signaling toward and within the nucleus (“nuclear calciopathy”), or increases in death signaling by extrasynaptic NMDA receptors.
DOI:doi:10.1523/JNEUROSCI.2672-10.2011
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext: https://doi.org/10.1523/JNEUROSCI.2672-10.2011
 Volltext: https://www.jneurosci.org/content/31/13/4978
 DOI: https://doi.org/10.1523/JNEUROSCI.2672-10.2011
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1831146096
Verknüpfungen:→ Zeitschrift

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