Trisomy-driven overexpression of DYRK1A kinase in the brain of subjects with Down syndrome
Author:
Publisher
Elsevier BV
Subject
General Neuroscience
Reference27 articles.
1. DYRK1A BAC transgenic mice show altered synaptic plasticity with learning and memory defects;Ahn;Neurobiol. Dis.,2006
2. Neurodevelopmental delay, motor abnormalities and cognitive deficits in transgenic mice overexpressing Dyrk1A (minibrain), a murine model of Down's syndrome;Altafaj;Hum. Mol. Gen.,2001
3. Dendritic atrophy in children with Down's syndrome;Becker;Ann. Neurol.,1986
4. Transgenic mouse in vivo library of human Down syndrome critical region 1: association between Dyrk1A overexpression, brain development abnormalities, and cell cycle protein alteration;Branchi;J. Neuropathol. Exp. Neurol.,2004
5. Dynamin is a minibrain kinase/dual specificity Yak1-related kinase 1A substrate;Chen-Hwang;J. Biol. Chem.,2002
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1. Analysis of microisolated frontal cortex excitatory layer III and V pyramidal neurons reveals a neurodegenerative phenotype in individuals with Down syndrome;Acta Neuropathologica;2024-08-06
2. Down syndrome and DYRK1A overexpression: relationships and future therapeutic directions;Frontiers in Molecular Neuroscience;2024-07-24
3. Dissecting the contribution of human chromosome 21 syntenic regions to recognition memory processes in adult and aged mouse models of Down syndrome;Frontiers in Behavioral Neuroscience;2024-07-10
4. Regulation of brain development by the Minibrain/Rala signaling network;2024-05-12
5. Psychoplastogenic DYRK1A Inhibitors with Therapeutic Effects Relevant to Alzheimer’s Disease;Journal of Medicinal Chemistry;2024-04-22
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