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anti-Human SHANK3 Anticorps:
anti-Rat (Rattus) SHANK3 Anticorps:
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Mammalian Monoclonal SHANK3 Primary Antibody pour ISt, IHC - ABIN1304955
Benthani, Tran, Currey, Ng, Giry-Laterriere, Carey, Kohonen-Corish, Pangon: Proteogenomic Analysis Identifies a Novel Human SHANK3 Isoform. dans International journal of molecular sciences 2015
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Rat (Rattus) Polyclonal SHANK3 Primary Antibody pour ICC, IHC - ABIN1742347
Tao-Cheng, Toy, Winters, Reese, Dosemeci: Zinc Stabilizes Shank3 at the Postsynaptic Density of Hippocampal Synapses. dans PLoS ONE 2016
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Mouse (Murine) Monoclonal SHANK3 Primary Antibody pour ICC, IHC - ABIN2115259
Duffney, Wei, Cheng, Liu, Smith, Kittler, Yan: Shank3 deficiency induces NMDA receptor hypofunction via an actin-dependent mechanism. dans The Journal of neuroscience : the official journal of the Society for Neuroscience 2013
Rat (Rattus) Monoclonal SHANK3 Primary Antibody pour ICC, IF - ABIN4353297
Mayanagi, Yasuda, Sobue: PSD-Zip70 Deficiency Causes Prefrontal Hypofunction Associated with Glutamatergic Synapse Maturation Defects by Dysregulation of Rap2 Activity. dans The Journal of neuroscience : the official journal of the Society for Neuroscience 2015
SHANK3 expression correlated with ZO-1 (Montrer TJP1 Anticorps) and PKCepsilon in colonic tissue of patients with Crohn's disease. The expre (Montrer TJP1 Anticorps)ssion level of SHANK (Montrer TJP1 Anticorps)3 affects ZO-1 expression and the barrier function in intestina (Montrer PRKCE Anticorps)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 (Montrer CHD8 Anticorps), and ADNP (Montrer ADNP Anticorps) 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 (Montrer ARSD Anticorps) at a locus in SHANK3.
SHANK1 (Montrer SHANK1 Anticorps) and SHANK3 act as integrin activation inhibitors by sequestering active Rap1 (Montrer RABGEF1 Anticorps) and R-Ras via the SPN (Montrer SPN Anticorps) domain and thus limiting their bioavailability at the plasma membrane.
Overexpression of SHANK3 enhanced ZO-1 (Montrer TJP1 Anticorps) expression, and knockdown of SHANK3 resulted in decreased expression of ZO-1 (Montrer TJP1 Anticorps). Regulation of ZO-1 (Montrer TJP1 Anticorps) expression by SHANK3 seems to be mediated through a PKCepsilon (Montrer PRKCE Anticorps)-dependent pathway. The expression level of SHANK3 affects ZO-1 (Montrer TJP1 Anticorps) 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 (Montrer GAD2 Anticorps)/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 (Montrer INADL Anticorps), 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 (Montrer SPN Anticorps) 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 (Montrer TRPV1 Anticorps)) via Proline-rich region and regulates TRPV1 (Montrer TRPV1 Anticorps) surface expression.
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