Shank3a/b isoforms regulate the susceptibility to seizures and thalamocortical development in the early postnatal period of mice

[1]  Prashant S. Emani,et al.  Broad transcriptomic dysregulation occurs across the cerebral cortex in ASD , 2022, Nature.

[2]  J. Leite,et al.  Parvalbumin Role in Epilepsy and Psychiatric Comorbidities: From Mechanism to Intervention , 2022, Frontiers in Integrative Neuroscience.

[3]  B. Leitch.  The Impact of Glutamatergic Synapse Dysfunction in the Corticothalamocortical Network on Absence Seizure Generation , 2022, Frontiers in Molecular Neuroscience.

[4]  Kenji F. Tanaka,et al.  Dysfunction of parvalbumin-expressing cells in the thalamic reticular nucleus induces cortical spike-and-wave discharges and an unconscious state , 2022, Brain communications.

[5]  C. Schaaf,et al.  Translational pediatrics: clinical perspective for Phelan–McDermid syndrome and autism research , 2021, Pediatric Research.

[6]  C. Akerman,et al.  Disrupting Epileptiform Activity by Preventing Parvalbumin Interneuron Depolarization Block , 2021, The Journal of Neuroscience.

[7]  Lijie Wu,et al.  Prevalence of epilepsy in autism spectrum disorders: A systematic review and meta-analysis , 2021, Autism : the international journal of research and practice.

[8]  D. Sasayama,et al.  Trends in Autism Spectrum Disorder Diagnoses in Japan, 2009 to 2019 , 2021, JAMA network open.

[9]  M. Avoli,et al.  4E-BP2–dependent translation in parvalbumin neurons controls epileptic seizure threshold , 2021, Proceedings of the National Academy of Sciences.

[10]  I. Vattulainen,et al.  SHANK3 conformation regulates direct actin binding and crosstalk with Rap1 signaling , 2021, Current Biology.

[11]  M. Kreutz,et al.  Autism-associated SHANK3 missense point mutations impact conformational fluctuations and protein turnover at synapses , 2021, bioRxiv.

[12]  Mingjie Zhang,et al.  CaMKIIα-driven, phosphatase-checked postsynaptic plasticity via phase separation , 2020, Cell Research.

[13]  H. Kreienkamp,et al.  Targeting of δ-catenin to postsynaptic sites through interaction with the Shank3 N-terminus , 2020, Molecular Autism.

[14]  Takahiro A. Kato,et al.  GNAO1 organizes the cytoskeletal remodeling and firing of developing neurons , 2020, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[15]  Luke A Allen,et al.  Thalamus and focal to bilateral seizures , 2020, Neurology.

[16]  C. Konradi,et al.  Parvalbumin interneuron vulnerability and brain disorders , 2020, Neuropsychopharmacology.

[17]  F. Kortüm,et al.  Truncating mutations in SHANK3 associated with global developmental delay interfere with nuclear β‐catenin signaling , 2020, Journal of neurochemistry.

[18]  Mingjie Zhang,et al.  Shank3 Binds to and Stabilizes the Active Form of Rap1 and HRas GTPases via Its NTD-ANK Tandem with Distinct Mechanisms. , 2019, Structure.

[19]  B. Leitch,et al.  The impact of silencing feed-forward parvalbumin-expressing inhibitory interneurons in the cortico-thalamocortical network on seizure generation and behaviour , 2019, Neurobiology of Disease.

[20]  B. Schwaller,et al.  Dysregulation of Parvalbumin Expression in the Cntnap2−/− Mouse Model of Autism Spectrum Disorder , 2018, Front. Mol. Neurosci..

[21]  Eunjoon Kim,et al.  Shank2 Deletion in Parvalbumin Neurons Leads to Moderate Hyperactivity, Enhanced Self-Grooming and Suppressed Seizure Susceptibility in Mice , 2018, Front. Mol. Neurosci..

[22]  Aaron E. L. Warren,et al.  Thalamocortical functional connectivity in Lennox–Gastaut syndrome is abnormally enhanced in executive‐control and default‐mode networks , 2017, Epilepsia.

[23]  B. Shyu,et al.  Suppression of cortical seizures by optic stimulation of the reticular thalamus in PV-mhChR2-YFP BAC transgenic mice , 2017, Molecular Brain.

[24]  Karl Deisseroth,et al.  Modulation of prefrontal cortex excitation/inhibition balance rescues social behavior in CNTNAP2-deficient mice , 2017, Science Translational Medicine.

[25]  Bo Zhang,et al.  Conditional Deletion of All Neurexins Defines Diversity of Essential Synaptic Organizer Functions for Neurexins , 2017, Neuron.

[26]  John R. Huguenard,et al.  Regulation of Thalamic and Cortical Network Synchrony by Scn8a , 2017, Neuron.

[27]  T. Boeckers,et al.  SHANK proteins limit integrin activation by directly interacting with Rap1 and R-Ras , 2017, Nature Cell Biology.

[28]  G. Feng,et al.  SHANK proteins: roles at the synapse and in autism spectrum disorder , 2017, Nature Reviews Neuroscience.

[29]  Michael M. C. Quach,et al.  The spectrum of epilepsy and electroencephalographic abnormalities due to SHANK3 loss‐of‐function mutations , 2016, Epilepsia.

[30]  H. Shigeto,et al.  Hyperactive mTOR signals in the proopiomelanocortin-expressing hippocampal neurons cause age-dependent epilepsy and premature death in mice , 2016, Scientific Reports.

[31]  S. Horvath,et al.  Shared molecular neuropathology across major psychiatric disorders parallels polygenic overlap , 2016, Science.

[32]  B. Schwaller,et al.  Reduction in parvalbumin expression not loss of the parvalbumin-expressing GABA interneuron subpopulation in genetic parvalbumin and shank mouse models of autism , 2016, Molecular Brain.

[33]  H. Zoghbi,et al.  Loss of MeCP2 in Parvalbumin-and Somatostatin-Expressing Neurons in Mice Leads to Distinct Rett Syndrome-like Phenotypes , 2015, Neuron.

[34]  R. Tuchman,et al.  Autism Spectrum Disorder and Epilepsy , 2015, Journal of child neurology.

[35]  Tristram H. Smith,et al.  Autism spectrum disorder and epilepsy: Disorders with a shared biology , 2015, Epilepsy & Behavior.

[36]  K. Futai,et al.  Shank1 regulates excitatory synaptic transmission in mouse hippocampal parvalbumin‐expressing inhibitory interneurons , 2015, The European journal of neuroscience.

[37]  Yoonji Lee,et al.  Transcriptional and functional complexity of Shank3 provides a molecular framework to understand the phenotypic heterogeneity of SHANK3 causing autism and Shank3 mutant mice , 2014, Molecular Autism.

[38]  Yi-Ju Li,et al.  Epigenetic dysregulation of SHANK3 in brain tissues from individuals with autism spectrum disorders. , 2014, Human molecular genetics.

[39]  A. Breman,et al.  SHANK3 overexpression causes manic-like behavior with unique pharmacogenetic properties , 2013, Nature.

[40]  D. Geschwind,et al.  Absence of CNTNAP2 Leads to Epilepsy, Neuronal Migration Abnormalities, and Core Autism-Related Deficits , 2011, Cell.

[41]  T. Bourgeron,et al.  SHANK3 mutations identified in autism lead to modification of dendritic spine morphology via an actin-dependent mechanism , 2011, Molecular Psychiatry.

[42]  G. Feng,et al.  Shank3 mutant mice display autistic-like behaviours and striatal dysfunction , 2011, Nature.

[43]  Mark J. Harris,et al.  Haploinsufficiency of the autism-associated Shank3 gene leads to deficits in synaptic function, social interaction, and social communication , 2010, Molecular autism.

[44]  Allen D. Delaney,et al.  Conserved Role of Intragenic DNA Methylation in Regulating Alternative Promoters , 2010, Nature.

[45]  T. Boeckers,et al.  Synaptic Cross-talk between N-Methyl-d-aspartate Receptors and LAPSER1-β-Catenin at Excitatory Synapses* , 2009, The Journal of Biological Chemistry.

[46]  M. Furuichi,et al.  MTH1, an Oxidized Purine Nucleoside Triphosphatase, Suppresses the Accumulation of Oxidative Damage of Nucleic Acids in the Hippocampal Microglia during Kainate-Induced Excitotoxicity , 2006, The Journal of Neuroscience.

[47]  P. Worley,et al.  Shank, a Novel Family of Postsynaptic Density Proteins that Binds to the NMDA Receptor/PSD-95/GKAP Complex and Cortactin , 1999, Neuron.

[48]  P. Rakic,et al.  Absence of excitotoxicity-induced apoptosis in the hippocampus of mice lacking the Jnk3 gene , 1997, Nature.

[49]  J. Bockmann,et al.  Synaptic Scaffolding Proteins in Rat Brain ANKYRIN REPEATS OF THE MULTIDOMAIN Shank PROTEIN FAMILY INTERACT WITH THE CYTOSKELETAL PROTEIN (cid:1) -FODRIN* , 2001 .