Datasheet

Biological Description

Specificity	SynGAP Antibody [F22M8] detects endogenous levels of total SynGAP protein.
Background	SynGAP (Synaptic Ras GTPase-Activating Protein 1), a brain-specific protein highly enriched at excitatory synapses in the mammalian forebrain, functions both as a negative regulator of Ras/ Rap GTPase signaling and as a structural component of postsynaptic densities (PSDs). It features an N-terminal pleckstrin homology (PH) domain and C2 domain for membrane association, a central RasGAP domain that accelerates Ras-GTP hydrolysis, a coiled-coil region for trimerization, and a C-terminal T/SXV motif binding PDZ domains of PSD-95/SAP102, coupling it to NMDA receptors. Phosphorylation by CaMKII at sites like Ser765/Ser1123 reduces PDZ binding affinity, dispersing SynGAP from PSDs and freeing PDZ slots (up to 15% occupied by SynGAP-α1) for AMPAR-TARP complexes, neuroligins, and LRRTMs to enhance synaptic strength. SynGAP restricts Ras/ERK signaling to limit AMPAR trafficking and stabilize immature synapses during development, while its activity-dependent dissociation promotes LTP by enabling surface AMPAR insertion and spine maturation. It also controls synaptic plasticity, spatial memory, and neuronal circuit excitability; SynGAP knockout mice exhibit postnatal lethality, impaired LTP, microcephaly, and cognitive deficits mirroring SYNGAP1-related disorders such as intellectual disability, autism, and epilepsy.

Specificity

SynGAP Antibody [F22M8] detects endogenous levels of total SynGAP protein.

Background

SynGAP (Synaptic Ras GTPase-Activating Protein 1), a brain-specific protein highly enriched at excitatory synapses in the mammalian forebrain, functions both as a negative regulator of Ras/ Rap GTPase signaling and as a structural component of postsynaptic densities (PSDs). It features an N-terminal pleckstrin homology (PH) domain and C2 domain for membrane association, a central RasGAP domain that accelerates Ras-GTP hydrolysis, a coiled-coil region for trimerization, and a C-terminal T/SXV motif binding PDZ domains of PSD-95/SAP102, coupling it to NMDA receptors. Phosphorylation by CaMKII at sites like Ser765/Ser1123 reduces PDZ binding affinity, dispersing SynGAP from PSDs and freeing PDZ slots (up to 15% occupied by SynGAP-α1) for AMPAR-TARP complexes, neuroligins, and LRRTMs to enhance synaptic strength. SynGAP restricts Ras/ERK signaling to limit AMPAR trafficking and stabilize immature synapses during development, while its activity-dependent dissociation promotes LTP by enabling surface AMPAR insertion and spine maturation. It also controls synaptic plasticity, spatial memory, and neuronal circuit excitability; SynGAP knockout mice exhibit postnatal lethality, impaired LTP, microcephaly, and cognitive deficits mirroring SYNGAP1-related disorders such as intellectual disability, autism, and epilepsy.

Usage Information

Application

WB, IHC, IF

Dilution

WB	IHC	IF
1:1000	1:400 - 1:1600	1:200 - 1:800

Reactivity

Mouse, Rat

Source

Rabbit Monoclonal Antibody

MW

140 kDa

Storage Buffer

PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage
(from the date of receipt)

-20°C (avoid freeze-thaw cycles), 2 years

References

https://pubmed.ncbi.nlm.nih.gov/32579114/
https://pubmed.ncbi.nlm.nih.gov/32075947/

SynGAP Antibody [F22M8]

Biological Description

Usage Information

References

Application Data