JNK signaling activation in the Ube3a maternal deficient mouse model: its specific inhibition prevents post-synaptic protein-enriched fraction alterations and cognitive deficits in Angelman Syndrome model-Reference-Cited by-同舟云学术

JNK signaling activation in the Ube3a maternal deficient mouse model: its specific inhibition prevents post-synaptic protein-enriched fraction alterations and cognitive deficits in Angelman Syndrome model

Published:2020-07 Issue: Volume:140 Page:104812
ISSN:0969-9961
Container-title:Neurobiology of Disease
language:en
Short-container-title:Neurobiology of Disease

Author:

Musi Clara Alice^ORCID,Agrò Graziella,Buccarello Lucia,Camuso Serena,Borsello Tiziana

Funder

Angelman Syndrome Alliance

Publisher

Elsevier BV

Subject

Neurology

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1. Imbalanced expression of cation-chloride cotransporters as a potential therapeutic target in an Angelman syndrome mouse model;Scientific Reports;2023-04-17

2. JNK Activation Correlates with Cognitive Impairment and Alteration of the Post-Synaptic Element in the 5xFAD AD Mouse Model;Cells;2023-03-15

3. Synaptic alterations as a common phase in neurological and neurodevelopmental diseases: JNK is a key mediator in synaptic changes;Neural Regeneration Research;2023

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5. Pathophysiological Significance of WDR62 and JNK Signaling in Human Diseases;Frontiers in Cell and Developmental Biology;2021-04-16