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anti-Human SHANK3 Antikörper:
anti-Rat (Rattus) SHANK3 Antikörper:
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Mammalian Monoclonal SHANK3 Primary Antibody für 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 für 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 für 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 für 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
SHANK3, CHD8 (zeige CHD8 Antikörper), and ADNP (zeige ADNP Antikörper) 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 (zeige ARSD Antikörper) at a locus in SHANK3.
SHANK1 (zeige SHANK1 Antikörper) and SHANK3 act as integrin activation inhibitors by sequestering active Rap1 (zeige RABGEF1 Antikörper) and R-Ras via the SPN (zeige SPN Antikörper) 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 (zeige LILRB1 Antikörper), miR (zeige MLXIP Antikörper)-34a, and miR (zeige MLXIP Antikörper)-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 (zeige LILRB1 Antikörper) 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
Results show that pairwise discrimination associative learning is disrupted in +/- Shank3B mice (heterozygous for exon 13-16, coding for the PDZ domain (zeige INADL Antikörper), 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 (zeige SPN Antikörper) 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 (zeige TRPV1 Antikörper)) via Proline-rich region and regulates TRPV1 (zeige TRPV1 Antikörper) 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 (zeige GRM5 Antikörper) signaling by regulating Homer (zeige HOMER1 Antikörper) recruitment/localization to the PSD (zeige PSD Antikörper) in brain regions that are highly associated with ASD (zeige GUSB Antikörper)-like behavior.
SHANK1 (zeige SHANK1 Antikörper) and SHANK3 act as integrin activation inhibitors by sequestering active Rap1 (zeige TERF2IP Antikörper) and R-Ras via the SPN (zeige SPN Antikörper) domain and thus limiting their bioavailability at the plasma membrane.
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 (zeige MEA1 Antikörper) recordings revealed electric phenotypes that displayed altered excitation and inhibition in the network lacking Shank3.
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