Postsynaptic ProSAP/Shank scaffolds in the cross-hair of synaptopathies.

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

[2]  Brain-Delivery of Zinc-Ions as Potential Treatment for Neurological Diseases: Mini Review. , 2011, Drug delivery letters.

[3]  A. Beaudet,et al.  Synaptic dysfunction and abnormal behaviors in mice lacking major isoforms of Shank3. , 2011, Human molecular genetics.

[4]  Jacqueline N. Crawley,et al.  Communication Impairments in Mice Lacking Shank1: Reduced Levels of Ultrasonic Vocalizations and Scent Marking Behavior , 2011, PloS one.

[5]  D. Linden,et al.  RETRACTED: Enhanced Polyubiquitination of Shank3 and NMDA Receptor in a Mouse Model of Autism , 2011, Cell.

[6]  Jacqueline N. Crawley,et al.  Sociability and motor functions in Shank1 mutant mice , 2011, Brain Research.

[7]  R. Huganir,et al.  Excess of de novo deleterious mutations in genes associated with glutamatergic systems in nonsyndromic intellectual disability. , 2011, American journal of human genetics.

[8]  Ann Tiiman,et al.  Interactions of Zn(II) and Cu(II) ions with Alzheimer's amyloid-beta peptide. Metal ion binding, contribution to fibrillization and toxicity. , 2011, Metallomics : integrated biometal science.

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

[10]  Danielle A. Simmons,et al.  Brief ampakine treatments slow the progression of Huntington's disease phenotypes in R6/2 mice , 2011, Neurobiology of Disease.

[11]  Michael R Kreutz,et al.  Concerted action of zinc and ProSAP/Shank in synaptogenesis and synapse maturation , 2011, The EMBO journal.

[12]  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.

[13]  Thomas Bourgeron,et al.  Key role for gene dosage and synaptic homeostasis in autism spectrum disorders. , 2010, Trends in genetics : TIG.

[14]  Gary D Bader,et al.  Functional impact of global rare copy number variation in autism spectrum disorders , 2010, Nature.

[15]  J. Yates,et al.  Progressive accumulation of amyloid‐β oligomers in Alzheimer’s disease and in amyloid precursor protein transgenic mice is accompanied by selective alterations in synaptic scaffold proteins , 2010, The FEBS journal.

[16]  Ute Moog,et al.  Mutations in the SHANK2 synaptic scaffolding gene in autism spectrum disorder and mental retardation , 2010, Nature Genetics.

[17]  Marie-Pierre Dubé,et al.  De novo mutations in the gene encoding the synaptic scaffolding protein SHANK3 in patients ascertained for schizophrenia , 2010, Proceedings of the National Academy of Sciences.

[18]  A. Bush,et al.  Cognitive Loss in Zinc Transporter-3 Knock-Out Mice: A Phenocopy for the Synaptic and Memory Deficits of Alzheimer's Disease? , 2010, The Journal of Neuroscience.

[19]  Q. Hong,et al.  Prefrontal cortex Homer expression in an animal model of attention-deficit/hyperactivity disorder , 2009, Journal of the Neurological Sciences.

[20]  Peter Faller,et al.  Copper and Zinc Binding to Amyloid‐β: Coordination, Dynamics, Aggregation, Reactivity and Metal‐Ion Transfer , 2009, Chembiochem : a European journal of chemical biology.

[21]  Andrea L. Rosso,et al.  Disruption of glutamate receptors at Shank-postsynaptic platform in Alzheimer's disease , 2009, Brain Research.

[22]  T. Kuner,et al.  Postsynaptic Neuroligin1 regulates presynaptic maturation , 2009, Proceedings of the National Academy of Sciences.

[23]  D. Richter,et al.  Fragile X Mental Retardation Protein Regulates the Levels of Scaffold Proteins and Glutamate Receptors in Postsynaptic Densities* , 2009, The Journal of Biological Chemistry.

[24]  Miou Zhou,et al.  Positive AMPA Receptor Modulation Rapidly Stimulates BDNF Release and Increases Dendritic mRNA Translation , 2009, The Journal of Neuroscience.

[25]  Takeshi Sakurai,et al.  The emerging role of synaptic cell-adhesion pathways in the pathogenesis of autism spectrum disorders , 2009, Trends in Neurosciences.

[26]  P. Livrea,et al.  Disassembly of Shank and Homer Synaptic Clusters Is Driven by Soluble β-Amyloid1-40 through Divergent NMDAR-Dependent Signalling Pathways , 2009, PloS one.

[27]  Inês Sousa,et al.  Copy number variation and association analysis of SHANK3 as a candidate gene for autism in the IMGSAC collection , 2009, European Journal of Human Genetics.

[28]  Laurent Mottron,et al.  Novel de novo SHANK3 mutation in autistic patients , 2009, American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics.

[29]  R. Metherate,et al.  A Role for Synaptic Zinc in Activity-Dependent Aβ Oligomer Formation and Accumulation at Excitatory Synapses , 2009, The Journal of Neuroscience.

[30]  Thomas Bourgeron,et al.  A synaptic trek to autism , 2009, Current Opinion in Neurobiology.

[31]  Huilin Li,et al.  The Postsynaptic Density Proteins Homer and Shank Form a Polymeric Network Structure , 2009, Cell.

[32]  E. Kandel,et al.  Neuroligin-1 is required for normal expression of LTP and associative fear memory in the amygdala of adult animals , 2008, Proceedings of the National Academy of Sciences.

[33]  D. Geschwind,et al.  Heterogeneous dysregulation of microRNAs across the autism spectrum , 2008, neurogenetics.

[34]  Shiaoching Gong,et al.  Minimal aberrant behavioral phenotypes of neuroligin‐3 R451C knockin mice , 2008, Autism research : official journal of the International Society for Autism Research.

[35]  M. C. Phelan.  Orphanet Journal of Rare Diseases BioMed Central Review Deletion 22q13.3 syndrome , 2008 .

[36]  Mark F Bear,et al.  Smaller Dendritic Spines, Weaker Synaptic Transmission, but Enhanced Spatial Learning in Mice Lacking Shank1 , 2008, The Journal of Neuroscience.

[37]  D. Pinto,et al.  Structural variation of chromosomes in autism spectrum disorder. , 2008, American journal of human genetics.

[38]  Christian R Marshall,et al.  Contribution of SHANK3 mutations to autism spectrum disorder. , 2007, American journal of human genetics.

[39]  Jacqueline Blundell,et al.  A Neuroligin-3 Mutation Implicated in Autism Increases Inhibitory Synaptic Transmission in Mice , 2007, Science.

[40]  T. Südhof,et al.  Activity-Dependent Validation of Excitatory versus Inhibitory Synapses by Neuroligin-1 versus Neuroligin-2 , 2007, Neuron.

[41]  C. Sala,et al.  DNA methylation regulates tissue‐specific expression of Shank3 , 2007, Journal of neurochemistry.

[42]  Thomas Bourgeron,et al.  Mutations in the gene encoding the synaptic scaffolding protein SHANK3 are associated with autism spectrum disorders , 2007, Nature Genetics.

[43]  C. Perrone-Capano,et al.  Short‐Term Effects of Adolescent Methylphenidate Exposure on Brain Striatal Gene Expression and Sexual/Endocrine Parameters in Male Rats , 2006, Annals of the New York Academy of Sciences.

[44]  G. Lynch,et al.  Synaptic plasticity in early aging , 2006, Ageing Research Reviews.

[45]  T. Boeckers,et al.  The postsynaptic density , 2006, Cell and Tissue Research.

[46]  J. Bowie,et al.  A role for zinc in postsynaptic density asSAMbly and plasticity? , 2006, TIBS -Trends in Biochemical Sciences. Regular ed.

[47]  Yasuko Nakamura,et al.  Direct interaction of post‐synaptic density‐95/Dlg/ZO‐1 domain‐containing synaptic molecule Shank3 with GluR1 α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole propionic acid receptor , 2006, Journal of neurochemistry.

[48]  G. Lynch.  Glutamate-based therapeutic approaches: ampakines. , 2006, Current opinion in pharmacology.

[49]  Eckart D Gundelfinger,et al.  An Architectural Framework That May Lie at the Core of the Postsynaptic Density , 2006, Science.

[50]  Min Goo Lee,et al.  Shank2 Associates with and Regulates Na+/H+ Exchanger 3* , 2006, Journal of Biological Chemistry.

[51]  H. Möhler.  GABAA Receptors in Central Nervous System Disease: Anxiety, Epilepsy, and Insomnia , 2006, Journal of receptor and signal transduction research.

[52]  R. Giorda,et al.  Identification of a recurrent breakpoint within the SHANK3 gene in the 22q13.3 deletion syndrome , 2005, Journal of Medical Genetics.

[53]  T. Hensch.  Critical period plasticity in local cortical circuits , 2005, Nature Reviews Neuroscience.

[54]  G. Edelman,et al.  Differential translation and fragile X syndrome , 2005, Genes, brain, and behavior.

[55]  B. Kampa,et al.  Synaptic integration in dendritic trees. , 2005, Journal of neurobiology.

[56]  J. Fridlyand,et al.  Epigenome analyses using BAC microarrays identify evolutionary conservation of tissue-specific methylation of SHANK3 , 2005, Nature Genetics.

[57]  P. Worley,et al.  Shank Expression Is Sufficient to Induce Functional Dendritic Spine Synapses in Aspiny Neurons , 2005, The Journal of Neuroscience.

[58]  P. Scheiffele,et al.  Control of Excitatory and Inhibitory Synapse Formation by Neuroligins , 2005, Science.

[59]  T. Boeckers,et al.  C‐terminal synaptic targeting elements for postsynaptic density proteins ProSAP1/Shank2 and ProSAP2/Shank3 , 2005, Journal of neurochemistry.

[60]  Mark Ellisman,et al.  A single mutation near the C-terminus in alpha/beta hydrolase fold protein family causes a defect in protein processing. , 2005, Chemico-biological interactions.

[61]  Nils Brose,et al.  The complexity of PDZ domain-mediated interactions at glutamatergic synapses: a case study on neuroligin , 2004, Neuropharmacology.

[62]  Yu Tian Wang,et al.  A balance between excitatory and inhibitory synapses is controlled by PSD-95 and neuroligin. , 2004, Proceedings of the National Academy of Sciences of the United States of America.

[63]  S. Schwartz,et al.  Terminal 22q deletion syndrome: a newly recognized cause of speech and language disability in the autism spectrum. , 2004, Pediatrics.

[64]  Mark F Bear,et al.  The mGluR theory of fragile X mental retardation , 2004, Trends in Neurosciences.

[65]  J. Bockmann,et al.  Differential expression and dendritic transcript localization of Shank family members: identification of a dendritic targeting element in the 3′ untranslated region of Shank1 mRNA , 2004, Molecular and Cellular Neuroscience.

[66]  Albert David,et al.  X-linked mental retardation and autism are associated with a mutation in the NLGN4 gene, a member of the neuroligin family. , 2004, American journal of human genetics.

[67]  H. Manev,et al.  DNA methylation as an epigenetic regulator of neural 5‐lipoxygenase expression: evidence in human NT2 and NT2‐N cells , 2004, Journal of neurochemistry.

[68]  Andrea Beckel-Mitchener,et al.  Correlates across the structural, functional, and molecular phenotypes of fragile X syndrome. , 2004, Mental retardation and developmental disabilities research reviews.

[69]  R. Malinow,et al.  Postsynaptic Density 95 controls AMPA Receptor Incorporation during Long-Term Potentiation and Experience-Driven Synaptic Plasticity , 2004, The Journal of Neuroscience.

[70]  H. Singer,et al.  Neurobiology of Tourette's syndrome: concepts of neuroanatomic localization and neurochemical abnormalities , 2003, Brain and Development.

[71]  L. Kochan,et al.  GABA and Schizophrenia: A Review of Basic Science and Clinical Studies , 2003, Journal of clinical psychopharmacology.

[72]  H. Zoghbi.  Postnatal Neurodevelopmental Disorders: Meeting at the Synapse? , 2003, Science.

[73]  M. Merzenich,et al.  Model of autism: increased ratio of excitation/inhibition in key neural systems , 2003, Genes, brain, and behavior.

[74]  G. Lynch,et al.  Chronic Elevation of Brain-Derived Neurotrophic Factor by Ampakines , 2003, Journal of Pharmacology and Experimental Therapeutics.

[75]  H. McDermid,et al.  Molecular characterisation of the 22q13 deletion syndrome supports the role of haploinsufficiency of SHANK3/PROSAP2 in the major neurological symptoms , 2003, Journal of medical genetics.

[76]  Thomas Bourgeron,et al.  Mutations of the X-linked genes encoding neuroligins NLGN3 and NLGN4 are associated with autism , 2003, Nature Genetics.

[77]  George Perry,et al.  Metal binding and oxidation of amyloid-beta within isolated senile plaque cores: Raman microscopic evidence. , 2003, Biochemistry.

[78]  T. Boeckers,et al.  ProSAP/Shank proteins – a family of higher order organizing molecules of the postsynaptic density with an emerging role in human neurological disease , 2002, Journal of neurochemistry.

[79]  M. Ehlers.  Molecular morphogens for dendritic spines , 2002, Trends in Neurosciences.

[80]  R. Borgatti,et al.  Disruption of the ProSAP2 gene in a t(12;22)(q24.1;q13.3) is associated with the 22q13.3 deletion syndrome. , 2001, American journal of human genetics.

[81]  Guosong Liu,et al.  Regulation of Dendritic Spine Morphology and Synaptic Function by Shank and Homer , 2001, Neuron.

[82]  C. Masters,et al.  Alzheimer's Disease Amyloid-β Binds Copper and Zinc to Generate an Allosterically Ordered Membrane-penetrating Structure Containing Superoxide Dismutase-like Subunits* , 2001, The Journal of Biological Chemistry.

[83]  R. Huganir,et al.  PDZ domains in synapse assembly and signalling. , 2000, Trends in cell biology.

[84]  M. Sheng,et al.  The Shank family of scaffold proteins. , 2000, Journal of cell science.

[85]  T. Boeckers,et al.  Proline-rich synapse-associated proteins ProSAP1 and ProSAP2 interact with synaptic proteins of the SAPAP/GKAP family. , 1999, Biochemical and biophysical research communications.

[86]  Eunjoon Kim,et al.  Characterization of the Shank Family of Synaptic Proteins , 1999, The Journal of Biological Chemistry.

[87]  T. Boeckers,et al.  Proline-Rich Synapse-Associated Protein-1/Cortactin Binding Protein 1 (ProSAP1/CortBP1) Is a PDZ-Domain Protein Highly Enriched in the Postsynaptic Density , 1999, The Journal of Neuroscience.

[88]  P. Worley,et al.  Coupling of mGluR/Homer and PSD-95 Complexes by the Shank Family of Postsynaptic Density Proteins , 1999, Neuron.

[89]  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.

[90]  G. Rogers,et al.  Synergistic interactions between ampakines and antipsychotic drugs. , 1999, The Journal of pharmacology and experimental therapeutics.

[91]  S. Weed,et al.  Identification of a Novel Cortactin SH3 Domain-Binding Protein and Its Localization to Growth Cones of Cultured Neurons , 1998, Molecular and Cellular Biology.

[92]  J. Massagué.  TGF-beta signal transduction. , 1998, Annual review of biochemistry.

[93]  M. Carlsson,et al.  Hypothesis: Is infantile autism a hypoglutamatergic disorder? Relevance of glutamate – serotonin interactions for pharmacotherapy , 1998, Journal of Neural Transmission.

[94]  J. Dumanski,et al.  Clinical, cytogenetic, and molecular characterization of seven patients with deletions of chromosome 22q13.3. , 1994, American journal of human genetics.

[95]  H. Wigström,et al.  Facilitated induction of hippocampal long-lasting potentiation during blockade of inhibition , 1983, Nature.