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The protein encoded by CACNG2 is a type I transmembrane AMPA receptor regulatory protein (TARP).
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Human Polyclonal CACNG2 Primary Antibody für WB - ABIN265040
Hofmann, Lacinová, Klugbauer: Voltage-dependent calcium channels: from structure to function. in Reviews of physiology, biochemistry and pharmacology 1999
Zeige alle 7 Referenzen für ABIN265040
Mouse (Murine) Polyclonal CACNG2 Primary Antibody für WB - ABIN372715
Tomita, Adesnik, Sekiguchi, Zhang, Wada, Howe, Nicoll, Bredt: Stargazin modulates AMPA receptor gating and trafficking by distinct domains. in Nature 2005
Mouse (Murine) Monoclonal CACNG2 Primary Antibody für ICC, IF - ABIN1686631
Khodosevich, Jacobi, Farrow, Schulmann, Rusu, Zhang, Sprengel, Monyer, von Engelhardt: Coexpressed auxiliary subunits exhibit distinct modulatory profiles on AMPA receptor function. in Neuron 2014
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 (zeige DLG4 Antikörper)) and stargazin, forming a ternary complex.
Region-specific differences investigated in GABAA (zeige GABRg1 Antikörper) receptor (GABAAR (zeige GABRG2 Antikörper)) 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 (zeige GRIA3 Antikörper) receptor auxiliary TARPg-2 subunit and the GluK5 (zeige GRIK1 Antikörper) subunit leads to early mouse lethality.
TARP gamma-2 was specifically expressed in cortical interneurons. Erbin (zeige ERBB2IP Antikörper) 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 (zeige CACNG7 Antikörper).
Results indicate that hippocampal and cerebellar long-term depression share a common pathway, namely dephosphorylation of stargazin by calcineurin (zeige PPP3CA Antikörper).
Ataxic phenotype in stargazers is primarily due to absence of AMPA (zeige GRIA3 Antikörper) receptors at cerebellar mossy-fiber-granule cell synapses.
Data suggest that stargazin interactions with and within the membrane play significant roles in TARP (zeige TINAGL1 Antikörper) structure and directly visualize TARP (zeige TINAGL1 Antikörper) functional mechanisms essential for AMPAR trafficking and clustering.
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 (zeige GRIA3 Antikörper) 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 (zeige GRIA3 Antikörper) receptor surface expression but also directly modulates AMPA (zeige GRIA3 Antikörper) receptor activity.
AMPA (zeige GRIA3 Antikörper) receptors complexed with stargazin are significantly more responsive to synaptically released glutamate (zeige GRIN1 Antikörper) compared with AMPA (zeige GRIA3 Antikörper) receptors lacking stargazin.
Stargazin enhances trafficking of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA (zeige GRIA3 Antikörper)) receptors GluR1 (zeige GRIA1 Antikörper) and GluR2 (zeige GRIA2 Antikörper) by blocking endoplasmic reticulum retention.
the Q/R site modulates the interaction of stargazin with the transmembrane domains of AMPA (zeige GRIA3 Antikörper) receptors via an allosteric mechanism and that this modulation leads to the observed differences in the electrophysiological properties of the receptor
Stargazin polymorphisms may play a role in the response to lithium treatment.
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