Anti-Shank3 Antibody (N69/46)

Our Anti-Shank3 mouse monoclonal primary antibody from NeuroMab is produced in-house from hybridoma clone N69/46. It detects human, mouse, and rat Shank3, and is purified by Protein A chromatography. It is great for use in IHC, ICC, IP, WB.



SKU: 75-109

Volume: 100 µL
Price:
Sale price$329.00
Ships: 1-2 business days

Product Details

Shank3
SH3 and multiple ankyrin repeat domains protein 3, or shank 3 (also known as proline-rich synapse-associated protein 2 (ProSAP2)) is a member of the shank family. Shank 3 binding domains include a SH3 domain, a proline rich domain, a PDZ domain and ankyrin repeat domains. Shank 3 is found in many tissues including heart and spleen, but is most abundantly expressed in brain at the post synaptic density. Shank 3 acts as a scaffold protein anchoring and connecting membrane bound receptors, ion channels and other proteins to the cytoskeleton in neurons to enable cell signaling. In this manner, Shank 3 may play a role in synapse formation and dendritic spine maturation. Mutations in the Shank 3 gene have been associated with neuropsychiatric diseases, including autism spectrm disorder.
Purified by Protein A chromatography
1 mg/mL
Monoclonal
N69/46
IgG2b
ICC, IHC, IP, WB
Mouse
Shank3 Prosap2
190 kDa
Synthetic peptide amino acids 840-857 (PEKLPGSLRKGIPRTKSV) of rat Shank3 (accession number Q9JLU4)
Human, Mouse, Rat
AB_2187730
Aliquot and store at ≤ -20°C for long term storage. For short term storage, store at 2-8°C. For maximum recovery of product, centrifuge the vial prior to removing the cap.
Liquid
Produced by in vitro bioreactor culture of hybridoma line followed by Protein A affinity chromatography. Purified mAbs are >90% specific antibody.
10 mM Tris, 50 mM Sodium Chloride, 0.065% Sodium Azide pH 7.37
WB: 1:1000
IHC: 1:500
ICC: 1:500
Unconjugated
No cross-reactivity against Shank1 or Shank2
Each new lot of antibody is quality control tested on cells overexpressing target protein and confirmed to give the expected staining pattern.
These antibodies are to be used as research laboratory reagents and are not for use as diagnostic or therapeutic reagents in humans.
United States
24 months from date of receipt
Shipped on ice packs
SH3 and multiple ankyrin repeat domains protein 3 (Shank3) (Proline-rich synapse-associated protein 2) (ProSAP2) (SPANK-2)

Product Specific References for Applications and Species

Immunocytochemistry: Human
PMID Dilution Publication
240894841:500Duffney LJ, et al. 2013. Shank3 deficiency induces NMDA receptor hypofunction via an actin-dependent mechanism.. Journal of Neuroscience, 15767-15778.
Immunocytochemistry: Rat
PMID Dilution Publication
21606927not listedDurand CM, et al. 2012. SHANK3 mutations identified in autism lead to modification of dendritic spine morphology via an actin-dependent mechanism.. Molecular Psychiatry, 71-84.
Immunohistochemistry: Human
PMID Dilution Publication
205731811:1000Pham E, et al. 2010. Progressive accumulation of amyloid-beta oligomers in Alzheimer's disease and in amyloid precursor protein transgenic mice is accompanied by selective alterations in synaptic scaffold proteins. FEBS Journal, 3051-3067.
Immunohistochemistry: Mouse
PMID Dilution Publication
25637745not listedBraude JP, et al. 2015. Deletion of Shank1 has minimal effects on the molecular composition and function of glutamatergic afferent postsynapses in the mouse inner ear.. Hearing Research, 52-64.
205731811:1000Pham E, et al. 2010. Progressive accumulation of amyloid-beta oligomers in Alzheimer's disease and in amyloid precursor protein transgenic mice is accompanied by selective alterations in synaptic scaffold proteins. FEBS Journal, 3051-3067.
Immuno-Gold: Rat
PMID Dilution Publication
262159191:10Farley MM, et al. 2015. Electron tomographic structure and protein composition of isolated rat cerebellar, hippocampal and cortical postsynaptic densities.. Neuroscience, 286-301.
Quantitative Multiplex Co-Immunoprecipitation: Mouse
PMID Dilution Publication
34852231not listedJonathan D Lautz, et al. 2021. Synaptic protein interaction networks encode experience by assuming stimulus-specific and brain-region-specific states. Cell Reports, 110076.
Western Blot: Human
PMID Dilution Publication
240894841:500Duffney LJ, et al. 2013. Shank3 deficiency induces NMDA receptor hypofunction via an actin-dependent mechanism.. Journal of Neuroscience, 15767-15778.
205731811:1000Pham E, et al. 2010. Progressive accumulation of amyloid-beta oligomers in Alzheimer's disease and in amyloid precursor protein transgenic mice is accompanied by selective alterations in synaptic scaffold proteins. FEBS Journal, 3051-3067.
Western Blot: Mouse
PMID Dilution Publication
384848631:1000Kelly-Castro, et al. 2024. MARK1 regulates dendritic spine morphogenesis and cognitive functions in vivo. Experimental Neurology, 114752.
289349771:1000Chhibber A, et al. 2017. ERβ and ApoE isoforms interact to regulate BDNF-5-HT2A signaling and synaptic function in the female brain. Alzheimers Research Therapy, 79.
26027926not listedDuffney LJ, et al. 2015. Autism-like Deficits in Shank3-Deficient Mice Are Rescued by Targeting Actin Regulators. Cell Reports, 1400-1413.
25997006not listedBenthani F, et al. 2015. Proteogenomic Analysis Identifies a Novel Human SHANK3 Isoform.. International Journal of Molecular Sciences, 11522-11530.
21167025not listedBozdagi O, et al. 2010. Haploinsufficiency of the autism-associated Shank3 gene leads to deficits in synaptic function, social interaction, and social communication.. Molecular Autism, 15.
205731811:1000Pham E, et al. 2010. Progressive accumulation of amyloid-beta oligomers in Alzheimer's disease and in amyloid precursor protein transgenic mice is accompanied by selective alterations in synaptic scaffold proteins. FEBS Journal, 3051-3067.
Western Blot: Rat
PMID Dilution Publication
281391981 : 100Harony-Nicolas H, et al. 2017. Oxytocin improves behavioral and electrophysiological deficits in a novel Shank3-deficient rat.. Elife, e18904.
21606927not listedDurand CM, et al. 2012. SHANK3 mutations identified in autism lead to modification of dendritic spine morphology via an actin-dependent mechanism.. Molecular Psychiatry, 71-84.

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