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GABRG2 encodes a gamma-aminobutyric acid (GABA) receptor. Additionally we are shipping GABRG2 Antibodies (117) and GABRG2 Proteins (4) and many more products for this protein.
This study identified a missense de novo mutation in the GABAA (show GABRg1 ELISA Kits) receptor gamma2 subunit, P302L, in a patient with Dravet syndrome. The mutation has a novel pathogenic mechanism to cause defects in the conductance and gating of GABAA (show GABRg1 ELISA Kits) receptors, which results in hyperexcitability and contributes to the pathogenesis of the genetic epilepsy Dravet syndrome.
This study demonstrated that rescue of PTZ seizure threshold and thalamocortical oscillations in a Gabrg2+/Q390X KI mouse model of Dravet syndrome/GEFS+ by overexpression of wild-type gamma2HA subunits.
Defects in GABRG2/GABAergic neurotransmission participate in the pathogenesis of genetic epilepsies including epileptic encephalopathies.
This review suggest that the pathogenesis of GABRG2 mutations is likely to be due to a combination of reduction of channel function and disturbance of cellular homeostasis due to the presence of mutant protein.
Nova1 (show NOVA1 ELISA Kits) interacts with GABAARgamma2 not only in the central nervous system but also in hepatocellular carcinoma. Nova1 (show NOVA1 ELISA Kits)'s potential mechanism as an oncogene (show RAB1A ELISA Kits) may due to its interaction with GABAA (show GABRg1 ELISA Kits) Rgamma2.
Thus, the presence of active GABA-A receptors, associated with phenotype determination via Ca(2 (show CA2 ELISA Kits)+)-signalling was demonstrated in differentiating human DA neurons.
common variants of GABRG2, RELN (show RELN ELISA Kits) and NRG3 (show NRG3 ELISA Kits) and the GABRG2-RELN (show RELN ELISA Kits)-PTCH1 (show PTCH1 ELISA Kits) interaction networks might confer altered susceptibility to Hirschsprung disease.
GABRG2, in combination with GABRA4 (show GABRA4 ELISA Kits), is associated with autism spectrum disorder in an Argentine dataset.
Deletion of the N-terminal extension and putative alpha-helix in heteromeric alpha1beta2gamma2 GABAA (show GABRg1 ELISA Kits) receptors in the gamma2 subunits reduced the number of functional receptors and incorporation into mature receptors.
Mutant GABRG2 may be responsible for genetic epilepsy as well neurodegeneration.
GABAA (show GABRg1 ELISA Kits) receptor (GABAAR) and the Na(+)-K(+)-2Cl(-) cotransporter (show SLC12A1 ELISA Kits) (NKCC1 (show SLC12A2 ELISA Kits)), but not the K(+)-Cl(-) cotransporter (show SLC12A4 ELISA Kits) (KCC2 (show SLC12A5 ELISA Kits)), were expressed in the terminals of the CRH (show CRH ELISA Kits) neurons at the median eminence (ME). In contrast, CRH (show CRH ELISA Kits) neuronal somata were enriched with KCC2 (show SLC12A5 ELISA Kits) but not with NKCC1 (show SLC12A2 ELISA Kits).
This study demonstrated that the reduced local input to fast-spiking interneurons in the somatosensory cortex in the GABAA (show GABRg1 ELISA Kits) gamma2 R43Q mouse model of absence epilepsy.
Heterozygous Gabrg2(+/Q390X) KI mice are associated with a severe epileptic encephalopathy due to a dominant negative effect of the mutation, while heterozygous Gabrg2(+/-) KO mice are associated with mild absence epilepsy due to simple haploinsufficiency.
This investigation demonstrates striking interfacial GABAA (show GABRg1 ELISA Kits) receptor subunit selectivity in the native milieu, suggesting that asymmetric occupancy of heteropentameric ion channels by alkylphenol-based anesthetics is sufficient to induce modulation of activity.
Study shows that the down-regulation of the gamma2 subunit of postsynaptic GABAARs in NG2 (show Vcan ELISA Kits) cells that accompanies the postnatal switch from synaptic to extrasynaptic GABAergic transmission between interneurons and these cells in the barrel cortex
Dendritic spine abnormalities of Gabrg2+/- mice suggest association of functional defects in glutamatergic transmission with the established anxious-depressive phenotype of these mice
KIF21B (show KIF21B ELISA Kits) participates in the delivery of GABAAR transport vesicles into dendrites.
The study demonstrates the molecular and functional diversity of the GABAAR system within the mouse colon providing a framework for developing GABAAR-based therapeutics in GI disorders.
these findings suggest that gephyrin (show GPHN ELISA Kits) may be a key factor in BDNF (show BDNF ELISA Kits)-dependent GABAAR regulation in the amygdala.
This study showed that oscillatory activity in thalamic circuits is under the control of inhibition that involves gamma2 subunit-independent GABA-ARs (show SLURP1 ELISA Kits)
This gene encodes a gamma-aminobutyric acid (GABA) receptor. GABA is the major inhibitory neurotransmitter in the mammlian brain, where it acts at GABA-A receptors, which are ligand-gated chloride channels. GABA-A receptors are pentameric, consisting of proteins from several subunit classes: alpha, beta, gamma, delta and rho. Mutations in this gene have been associated with epilepsy and febrile seizures. Multiple transcript variants encoding different isoforms have been identified for this gene.
gamma-aminobutyric acid A receptor, gamma 1
, GABA(A) receptor subunit gamma-2
, gamma-aminobutyric acid receptor subunit gamma-2
, gamma-aminobutyric acid A receptor gamma 2
, gamma-aminobutyric acid (GABA) A receptor, gamma 2
, gamma-aminobutyric acid receptor subunit gamma-2-like
, gamma-aminobutyric acid A receptor, gamma 2
, gamma-aminobutyric acid (GABA-A) receptor, subunit gamma 2
, gamma-aminobutyric acid A receptor, gamma 2
, GABA-A receptor gamma-2 subunit
, GABA(A) receptor, gamma 2