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anti-Human SHANK3 Antibodies:
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Mammalian Monoclonal SHANK3 Primary Antibody for ISt, IHC - ABIN1304955
Benthani, Tran, Currey, Ng, Giry-Laterriere, Carey, Kohonen-Corish, Pangon: Proteogenomic Analysis Identifies a Novel Human SHANK3 Isoform. in International journal of molecular sciences 2015
Show all 8 Pubmed References
Rat (Rattus) Polyclonal SHANK3 Primary Antibody for ICC, IHC - ABIN1742347
Tao-Cheng, Toy, Winters, Reese, Dosemeci: Zinc Stabilizes Shank3 at the Postsynaptic Density of Hippocampal Synapses. in PLoS ONE 2016
Show all 4 Pubmed References
Mouse (Murine) Monoclonal SHANK3 Primary Antibody for ICC, IHC - ABIN2115259
Duffney, Wei, Cheng, Liu, Smith, Kittler, Yan: Shank3 deficiency induces NMDA receptor hypofunction via an actin-dependent mechanism. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2013
Rat (Rattus) Monoclonal SHANK3 Primary Antibody for ICC, IF - ABIN4353297
Mayanagi, Yasuda, Sobue: PSD-Zip70 Deficiency Causes Prefrontal Hypofunction Associated with Glutamatergic Synapse Maturation Defects by Dysregulation of Rap2 Activity. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2015
shank3b-/- zebrafish displayed robust autism-like behaviors and altered levels of the synaptic proteins homer1 and synaptophysin.
Both syngap1b and shank3a play novel roles in morphogenesis resulting in common brain and behavioral phenotypes.
Results showed decreased expression of Zn uptake transporters ZIP2 and ZIP4 on mRNA and protein level correlating with SHANK3 expression levels, and found reduced levels of ZIP4 protein co-localizing with SHANK3 at the plasma membrane. ZIP4 exists in a complex with SHANK3. Further results confirmed a link between enterocytic SHANK3, ZIP2 and ZIP4.
SHANK3 haploinsufficiency due to point mutations alone is sufficient to cause a broad range of phenotypic features associated with Phelan-McDermid syndrome.
Our report details a 10-year-old boy with a de novo heterozygous c.1231del, p.Arg411Val frameshift variant in SHANK3, a high-risk candidate autism gene. We report significant speech delay and seizures as an association with this phenotype.
SHANK3 expression correlated with ZO-1 and PKCepsilon in colonic tissue of patients with Crohn's disease. The expression level of SHANK3 affects ZO-1 expression and the barrier function in intestinal epithelial cells.
We report a family with four affected individuals including the 37 year-old mother, her 12 year-old male monozygotic twins and 8 year-old daughter harboring a novel SHANK3 interstitial microdeletion
the present study did not provide evidences to support the fact that SHANK3 variants could influence the susceptibility to Autism spectrum disorder in the Northeastern Han Chinese population
SHANK3 expression was increased in the neocortex of temporal lobe epilepsy patients and rats.
Missense mutation in SHANK3 gene is associated with schizophrenia.
This study does not provide evidence for a major role of SHANK3 in the pathogenesis of bipolar disorder.
SHANK3, CHD8, and ADNP had distinctly higher scores than all other genes in the dataset describing the genes associated with autism spectrum disorders.
Partial knockdown of SHANK3 expression in human dorsal root ganglion neurons abrogates TRPV1 function.
GWA study identified maternal genetic effects not previously identified in ASD at a locus in SHANK3.
SHANK1 and SHANK3 act as integrin activation inhibitors by sequestering active Rap1 and R-Ras via the SPN domain and thus limiting their bioavailability at the plasma membrane.
No specific EEG abnormality is present in epilepsy due to to SHANK3 loss-of-function mutations.
Haploinsufficiency of SHANK3 is a predisposing factor in adults with catatonia.
post-transcriptional regulation of SHANK3 expression by three microRNAs (miRNAs), miR-7, miR-34a, and miR-504, is reported.
these data suggest that SHANK3 mutations predispose to autism, at least partially, by inducing an Ih channelopathy that may be amenable to pharmacological intervention.
De novo SHANK3 mutation causes Rett syndrome-like phenotype in a female patient.
miR-7 binds to 3-prime untranslated regions of SHANK3 mRNA and causes the alteration of neuronal morphology and function, potentially playing a crucial role in the pathophysiological process of schizophrenia
a mutation in SHANK3 that underscores its relevance in Autism Spectrum Disorder.
These results suggest spontaneous seizure and partial lethality of juvenile Shank3 transgenic mice in seizure-resistant background, further supporting the validity of this model.
The study supports a dissociation of Shank3 functions in cortical and striatal neurons in autism spectrum disease-related behaviors, and it illustrates the complexity of neural circuit mechanisms underlying these behaviors.
Describe a complete knockout mouse model of the autism-associated Shank3 gene, with a deletion of exons 4-22 (Deltae4-22). Both mGluR5-Homer scaffolds and mGluR5-mediated signalling are selectively altered in striatal neurons. These changes are associated with perturbed function at striatal synapses, abnormal brain morphology, aberrant structural connectivity and autism spectrum disorder-like behaviour.
The Shank3/F model, and to a much lesser extent, the Shank3/J and Cacna1c models, showed hypoactivity and a general anxiety-like behavior triggered by external stimuli which pervaded social interactions.
Overexpression of SHANK3 enhanced ZO-1 expression, and knockdown of SHANK3 resulted in decreased expression of ZO-1. Regulation of ZO-1 expression by SHANK3 seems to be mediated through a PKCepsilon-dependent pathway. The expression level of SHANK3 affects ZO-1 expression and the barrier function in intestinal epithelial cells in mice.
Mutations/deletions in the SHANK3 gene are associated with autism spectrum disorders and intellectual disability.
Results suggest age-dependent decrease of GAD65/67 mRNAs but normal densities of certain GABAergic interneurons in the Shank3 transgenic mice.
In a Shank3 Deltaex(4-9) mouse model the excitatory synaptic transmission within the ventral tegmental area is not affected.
Together, our results showing that zinc affected the Shank3 protein interactions of in vitro mouse synaptosomes provided an additional link between zinc and core synaptic proteins that have been implicated in multiple brain disorders.
Results show that pairwise discrimination associative learning is disrupted in +/- Shank3B mice (heterozygous for exon 13-16, coding for the PDZ domain, deletion), opening a new pathway to study neurobiological mechanisms behind intellectual disabilities caused by deletions/mutations in SHANK3.
Shank3 deletion preferentially affects synapses onto striatopallidal MSNs. Striatopallidal MSNs showed profound defects, including alterations in synaptic transmission, synaptic plasticity, and spine density.
a mouse model of autism with deletions in Shank3 (Shank3B-/-) shows early cortical hyperactivity, which triggers increased SPN excitatory synapse and corticostriatal hyperconnectivity.
used shRNA to model Shank3 insufficiency in the ventral tegmental area of mice
Homozygous and heterozygous Shank3 complete knockout (Deltae4-22) results in impaired heat hyperalgesia in inflammatory and neuropathic pain. SHANK3 interacts with transient receptor potential subtype V1 (TRPV1) via Proline-rich region and regulates TRPV1 surface expression.
we characterized the behavioral, molecular and electrophysiological phenotypes of Shank3 mutant mice that were generated by deleting exon 11. The results of our molecular studies further indicate that Shank3 plays a major role in modulating mGlu5 signaling by regulating Homer recruitment/localization to the PSD in brain regions that are highly associated with ASD-like behavior.
In the hippocampus, changes in synaptic Shank3 levels are influenced by circadian rhythm/melatonin concentration, while running activity increases and decreases levels of Shank3 in the cortex and striatum respectively
Shank3 is a multi-domain, synaptic scaffolding protein that organizes proteins in the postsynaptic density of excitatory synapses.
Cortical neurons cultured on MEAs displayed a rich repertoire of spontaneous firing, and Shank3 deletion led to reduced firing. MEA recordings revealed electric phenotypes that displayed altered excitation and inhibition in the network lacking Shank3.
"reduction of PV(+) neurons" was in all cases, i.e., in PV+/-, Shank1-/- and Shank3B-/- mice, was due to a reduction in Pvalb mRNA and PV protein.
This gene is a member of the Shank gene family. Shank proteins are multidomain scaffold proteins of the postsynaptic density that connect neurotransmitter receptors, ion channels, and other membrane proteins to the actin cytoskeleton and G-protein-coupled signaling pathways. Shank proteins also play a role in synapse formation and dendritic spine maturation. Mutations in this gene are a cause of autism spectrum disorder (ASD), which is characterized by impairments in social interaction and communication, and restricted behavioral patterns and interests. Mutations in this gene also cause schizophrenia type 15, and are a major causative factor in the neurological symptoms of 22q13.3 deletion syndrome, which is also known as Phelan-McDermid syndrome. Additional isoforms have been described for this gene but they have not yet been experimentally verified.
SH3 and multiple ankyrin repeat domains 3
, SH3 and multiple ankyrin repeat domains protein 3-like
, SH3 and multiple ankyrin repeat domains protein 3
, proline rich synapse associated protein 2
, shank postsynaptic density protein
, SH3/ankyrin domain gene 3
, Shank postsynaptic density protein 3a
, proline-rich synapse-associated protein 2
, SH3 and multiple ankyrin repeat domains-like protein 3 variant 1
, SH3 and multiple ankyrin repeat domains-like protein 3 variant 2
, SH3 and multiple ankyrin repeat domains-like protein 3 variant 3
, SH3 and multiple ankyrin repeat domains-like protein 3 variant d-1