SHANK3 blocking peptide

Name: SHANK3 blocking peptide
SKU: CDBP6094
Rating: 5 (1 reviews)

Synthetic SHANK3 blocking peptide for IB

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COA

SDS

Datasheet

Nature

Synthetic

Tag/Conjugate

Unconjugated

Format

Liquid

Concentration

200 μg/mL

Preservative

None

Storage

-20°C

Gene ID

85358

UniProt ID

Q9BYB0

Antigen Description

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. [provided by RefSeq, Mar 2012]

Function

GKAP/Homer scaffold activity; SH3 domain binding; actin binding; identical protein binding; ionotropic glutamate receptor binding; protein C-terminus binding; protein binding; scaffold protein binding; zinc ion binding

Synonyms

SHANK3; SH3 and multiple ankyrin repeat domains 3; PSAP2; SCZD15; PROSAP2; SPANK-2; DEL22q13.3; SH3 and multiple ankyrin repeat domains protein 3; shank postsynaptic density protein; proline rich synapse associated protein 2

Citations

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Customer Reviews

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Social deficits in Shank3-deficient mouse models of autism are rescued by histone deacetylase (HDAC) inhibition (vol 21, pg 564, 2018)

NATURE NEUROSCIENCE

Authors: Qin, Luye; Ma, Kaijie; Wang, Zi-Jun; Hu, Zihua; Matas, Emmanuel; Wei, Jing; Yan, Zhen

Abstract

Autism-Associated Insertion Mutation (InsG) of Shank3 Exon 21 Causes Impaired Synaptic Transmission and Behavioral Deficits

JOURNAL OF NEUROSCIENCE

Authors: Speed, Haley E.; Kouser, Mehreen; Xuan, Zhong; Reimers, Jeremy M.; Ochoa, Christine F.; Gupta, Natasha; Liu, Shunan; Powell, Craig M.

Abstract

SHANK3 (also known as PROSAP2) is a postsynaptic scaffolding protein at excitatory synapses in which mutations and deletions have been implicated in patients with idiopathic autism, Phelan-McDermid (aka 22q13 microdeletion) syndrome, and other neuropsychiatric disorders. In this study, we have created a novel mouse model of human autism caused by the insertion of a single guanine nucleotide into exon 21 (Shank3(G)). The resulting frameshift causes a premature STOP codon and loss of major higher molecular weight Shank3 isoforms at the synapse. Shank3(G/G) mice exhibit deficits in hippocampus-dependent spatial learning, impaired motor coordination, altered response to novelty, and sensory processing deficits. At the cellular level, Shank3(G/G) mice also exhibit impaired hippocampal excitatory transmission and plasticity as well as changes in baseline NMDA receptor-mediated synaptic responses. This work identifies clear alterations in synaptic function and behavior in a novel, genetically accurate mouse model of autism mimicking an autism-associated insertion mutation. Furthermore, these findings lay the foundation for future studies aimed to validate and study region-selective and temporally selective genetic reversal studies in the Shank3(G/G) mouse that was engineered with such future experiments in mind.