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anti-Human SHANK3 Antikörper:
anti-Rat (Rattus) SHANK3 Antikörper:
anti-Mouse (Murine) 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
shank3b-/- zebrafish displayed robust autism-like behaviors and altered levels of the synaptic proteins homer1 (zeige HOMER1 Antikörper) and synaptophysin (zeige SYP Antikörper).
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 (zeige TJP1 Antikörper) and PKCepsilon in colonic tissue of patients with Crohn's disease. The expre (zeige TJP1 Antikörper)ssion level of SHANK (zeige TJP1 Antikörper)3 affects ZO-1 expression and the barrier function in intestina (zeige PRKCE Antikörper)l 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 (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.
Describe a complete knockout mouse model of the autism-associated Shank3 gene, with a deletion of exons 4-22 (Deltae4-22). Both mGluR5 (zeige GRM5 Antikörper)-Homer (zeige HOMER1 Antikörper) scaffolds and mGluR5 (zeige GRM5 Antikörper)-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 (zeige CACNA1C Antikörper) models, showed hypoactivity and a general anxiety-like behavior triggered by external stimuli which pervaded social interactions.
Overexpression of SHANK3 enhanced ZO-1 (zeige TJP1 Antikörper) expression, and knockdown of SHANK3 resulted in decreased expression of ZO-1 (zeige TJP1 Antikörper). Regulation of ZO-1 (zeige TJP1 Antikörper) expression by SHANK3 seems to be mediated through a PKCepsilon (zeige PRKCE Antikörper)-dependent pathway. The expression level of SHANK3 affects ZO-1 (zeige TJP1 Antikörper) 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 (zeige GAD2 Antikörper)/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 (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.
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