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抗Human SHANK3 抗体:
抗Rat (Rattus) SHANK3 抗体:
抗Mouse (Murine) SHANK3 抗体:
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
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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
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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
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
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 (显示 CHD8 抗体), and ADNP (显示 ADNP 抗体) 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 (显示 ARSD 抗体) at a locus in SHANK3.
SHANK1 (显示 SHANK1 抗体) and SHANK3 act as integrin activation inhibitors by sequestering active Rap1 (显示 RABGEF1 抗体) and R-Ras via the SPN (显示 SPN 抗体) 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.
Mutations/deletions in the SHANK3 gene are associated with autism spectrum disorders and intellectual disability.
Results suggest age-dependent decrease of GAD65 (显示 GAD2 抗体)/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 (显示 INADL 抗体), 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 (显示 SPN 抗体) 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 (显示 TRPV1 抗体)) via Proline-rich region and regulates TRPV1 (显示 TRPV1 抗体) 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 (显示 GRM5 抗体) signaling by regulating Homer (显示 HOMER1 抗体) recruitment/localization to the PSD (显示 PSD 抗体) in brain regions that are highly associated with ASD (显示 GUSB 抗体)-like behavior.
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