Unexpected Compensatory Increase in Shank3 Transcripts in Shank3 Knock-Out Mice Having Partial Deletions of Exons
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Title
Unexpected Compensatory Increase in Shank3 Transcripts in Shank3 Knock-Out Mice Having Partial Deletions of Exons
Authors
Keywords
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Journal
Frontiers in Molecular Neuroscience
Volume 12, Issue -, Pages -
Publisher
Frontiers Media SA
Online
2019-09-19
DOI
10.3389/fnmol.2019.00228
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- (2018) Meghan Kerrisk Campbell et al. JOURNAL OF NEUROSCIENCE
- Social deficits in Shank3-deficient mouse models of autism are rescued by histone deacetylase (HDAC) inhibition
- (2018) Luye Qin et al. NATURE NEUROSCIENCE
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- (2018) Fatemeh Hassani Nia et al. Frontiers in Molecular Neuroscience
- Integrative Brain Transcriptome Analysis Reveals Region-Specific and Broad Molecular Changes in Shank3-Overexpressing Mice
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- Early Correction of N-Methyl-D-Aspartate Receptor Function Improves Autistic-like Social Behaviors in Adult Shank2−/− Mice
- (2018) Changuk Chung et al. BIOLOGICAL PSYCHIATRY
- Spontaneous seizure and partial lethality of juvenile Shank3-overexpressing mice in C57BL/6 J background
- (2018) Chunmei Jin et al. Molecular Brain
- Transcriptome analysis of Shank3-overexpressing mice reveals unique molecular changes in the hypothalamus
- (2018) Chunmei Jin et al. Molecular Brain
- SHANK proteins limit integrin activation by directly interacting with Rap1 and R-Ras
- (2017) Johanna Lilja et al. NATURE CELL BIOLOGY
- SHANK proteins: roles at the synapse and in autism spectrum disorder
- (2017) Patricia Monteiro et al. NATURE REVIEWS NEUROSCIENCE
- Age-dependent decrease of GAD65/67 mRNAs but normal densities of GABAergic interneurons in the brain regions of Shank3 -overexpressing manic mouse model
- (2017) Bokyoung Lee et al. NEUROSCIENCE LETTERS
- Striatal Transcriptome and Interactome Analysis of Shank3-overexpressing Mice Reveals the Connectivity between Shank3 and mTORC1 Signaling
- (2017) Yeunkum Lee et al. Frontiers in Molecular Neuroscience
- Integrative Analysis of Brain Region-specific Shank3 Interactomes for Understanding the Heterogeneity of Neuronal Pathophysiology Related to SHANK3 Mutations
- (2017) Yeunkum Lee et al. Frontiers in Molecular Neuroscience
- Bipolar Disorder Associated microRNA, miR-1908-5p, Regulates the Expression of Genes Functioning in Neuronal Glutamatergic Synapses
- (2016) Yoonhee Kim et al. Experimental Neurobiology
- Shank3-mutant mice lacking exon 9 show altered excitation/inhibition balance, enhanced rearing, and spatial memory deficit
- (2015) Jiseok Lee et al. Frontiers in Cellular Neuroscience
- Post-transcriptional regulation of SHANK3 expression by microRNAs related to multiple neuropsychiatric disorders
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- Phenotypic and functional analysis of SHANK3 stop mutations identified in individuals with ASD and/or ID
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- Fragile X-like behaviors and abnormal cortical dendritic spines in Cytoplasmic FMR1-interacting protein 2-mutant mice
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- Transcriptional and functional complexity of Shank3 provides a molecular framework to understand the phenotypic heterogeneity of SHANK3 causing autism and Shank3 mutant mice
- (2014) Xiaoming Wang et al. Molecular Autism
- Human-specific regulation of MeCP2 levels in fetal brains by microRNA miR-483-5p
- (2013) K. Han et al. GENES & DEVELOPMENT
- Epigenetic dysregulation of SHANK3 in brain tissues from individuals with autism spectrum disorders
- (2013) Li Zhu et al. HUMAN MOLECULAR GENETICS
- Loss of Predominant Shank3 Isoforms Results in Hippocampus-Dependent Impairments in Behavior and Synaptic Transmission
- (2013) M. Kouser et al. JOURNAL OF NEUROSCIENCE
- SHANK3 overexpression causes manic-like behaviour with unique pharmacogenetic properties
- (2013) Kihoon Han et al. NATURE
- Modeling Autism by SHANK Gene Mutations in Mice
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- Synaptic dysfunction and abnormal behaviors in mice lacking major isoforms of Shank3
- (2011) Xiaoming Wang et al. HUMAN MOLECULAR GENETICS
- Shank3 mutant mice display autistic-like behaviours and striatal dysfunction
- (2011) João Peça et al. NATURE
- Postsynaptic ProSAP/Shank scaffolds in the cross-hair of synaptopathies
- (2011) Andreas M. Grabrucker et al. TRENDS IN CELL BIOLOGY
- Haploinsufficiency of the autism-associated Shank3 gene leads to deficits in synaptic function, social interaction, and social communication
- (2011) Ozlem Bozdagi et al. Molecular Autism
- The Postsynaptic Density Proteins Homer and Shank Form a Polymeric Network Structure
- (2009) Mariko Kato Hayashi et al. CELL
- Regulated RalBP1 Binding to RalA and PSD-95 Controls AMPA Receptor Endocytosis and LTD
- (2009) Kihoon Han et al. PLOS BIOLOGY
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