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Study shows the expression of the TARP gamma2 in a non-mammalian vertebrate, and reveals a functional role for Cacng2a in synaptic physiology and development; suggests that Cacng2a is required for normal trafficking and function of synaptic AMPARs, while Cacng2b is largely non-functional with respect to the development of AMPA (show GRIA3 ELISA Kits) synaptic transmission
show that upon release of glutamate (show GRIN1 ELISA Kits), synaptic AMPARs were desensitized by transmitter by >90%. As glutamate (show GRIN1 ELISA Kits) levels subsequently fell, recovery of transmission occurred due to the presence of the AMPAR accessory protein stargazin that enhances the AMPAR response to low levels of transmitter.
we show that the TARP gamma-2 (stargazin) is present in spinal dorasl horn neurons and is necessary in a form of inflammatory pain-induced plasticity
the density of AMPARs correlates with that of TARP gamma-2 across SCC (show CYP11A1 ELISA Kits) synapses and its high expression is linked to high-density AMPAR expression at perforated type of pyramidal cell synapses
in the absence of stargazin, the refinement of the retinogeniculate synapse is specifically disrupted during the experience-dependent phase. Stargazin expression and phosphorylation increased with visual deprivation.
SR interacts with the synaptic proteins, postsynaptic density protein 95 (PSD-95 (show DLG4 ELISA Kits)) and stargazin, forming a ternary complex.
Region-specific differences investigated in GABAA (show GABRg1 ELISA Kits) receptor (GABAAR (show GABRG2 ELISA Kits)) subunit expression occur in the ventral posterior and reticular thalamic nucleus regions in the stargazer mouse model of absence epilepsy.
The combined loss of the AMPA (show GRIA3 ELISA Kits) receptor auxiliary TARPg-2 subunit and the GluK5 (show GRIK1 ELISA Kits) subunit leads to early mouse lethality.
TARP gamma-2 was specifically expressed in cortical interneurons. Erbin (show ERBB2IP ELISA Kits) interacts with TARP gamma-2 and is crucial for its stability.
This study suggested that, in stg, a trafficking defect in synaptic AMPARs in RTN cells leads to a compensatory increase in synaptic NMDARs and enhanced thalamic excitability.
the loss of gamma-2 in stargazer mouse stellate cells induces changes in synaptic transmission that cannot be compensated for by the remaining TARP gamma-7 (show CACNG7 ELISA Kits).
In addition to changes in MEK3 (show MAP2K3 ELISA Kits) gene regulation, our study demonstrated upregulation of CACNG2 and GADD45G (show GADD45G ELISA Kits) at the mRNA level in CMM patients.
A transient positive feedback mechanism between AMPAR and stargazin has implications for information processing in the brain, because it should allow activity-dependent facilitation of excitatory synaptic transmission through a postsynaptic mechanism.
The additional cleft closure and/or stabilization of the more closed-cleft states of the LBD is expected to translate to higher agonist efficacy and could contribute to the structural mechanism for stargazin modulation of AMPAR function.
Autoinactivation is a subunit and splice form dependent property of AMPA (show GRIA3 ELISA Kits) receptor-stargazin complexes, which involves structural rearrangements within the complex rather than any physical dissociation.
Susceptibility to chronic pain following nerve injury is genetically affected by CACNG2
examined distribution of the stargazin-like proteins gamma2, gamma3, and gamma4 in human CNS: gamma2 is expressed in cerebellum, cerebral cortex, hippocampus and thalamus, whereas gamma3 abounds in cerebral cortex & amygdala and gamma4 in basal ganglia
These results suggest that stargazin (gamma-2) not only promotes AMPA (show GRIA3 ELISA Kits) receptor surface expression but also directly modulates AMPA (show GRIA3 ELISA Kits) receptor activity.
AMPA (show GRIA3 ELISA Kits) receptors complexed with stargazin are significantly more responsive to synaptically released glutamate (show GRIN1 ELISA Kits) compared with AMPA (show GRIA3 ELISA Kits) receptors lacking stargazin.
Stargazin enhances trafficking of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA (show GRIA3 ELISA Kits)) receptors GluR1 (show GRIA1 ELISA Kits) and GluR2 (show GRIA2 ELISA Kits) by blocking endoplasmic reticulum retention.
the Q/R site modulates the interaction of stargazin with the transmembrane domains of AMPA (show GRIA3 ELISA Kits) receptors via an allosteric mechanism and that this modulation leads to the observed differences in the electrophysiological properties of the receptor
The protein encoded by this gene is a type I transmembrane AMPA receptor regulatory protein (TARP). TARPs regulate both trafficking and channel gating of the AMPA receptors. This gene is part of a functionally diverse eight-member protein subfamily of the PMP-22/EMP/MP20 family. This gene is a susceptibility locus for schizophrenia.
voltage-dependent calcium channel gamma-2 subunit
, calcium channel, voltage-dependent, gamma subunit 2
, TARP gamma 2
, TARP gamma-2
, neuronal voltage-gated calcium channel gamma-2 subunit
, transmembrane AMPAR regulatory protein gamma-2