SynGAP Antibody [F22M8] | Primary Antibodies

Application: Reactivity: Mouse, Rat

Usage Information

Dilution
WB1:1000 IHC1:400 - 1:1600 IF1:200 - 1:800

Application
WB, IHC, IF

Reactivity
Mouse, Rat

Source
Rabbit Monoclonal Antibody

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

Predicted MW
140 kDa

Datasheet & SDS

Biological Description

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

Clone
F22M8

Synonym(s)
DKFZp761G1421; KIAA1938; MRD5; Neuronal RasGAP; Ras GTPase-activating protein SynGAP; Ras/Rap GTPase-activating protein SynGAP; RASA1; RASA5; SYGP1; synaptic Ras GTPase activating protein, 135kDa; SYNGAP; SYNGAP1

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.

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.

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

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%