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GABRA4 is associated with autism spectrum disorder in a dataset from Argentina.
Transgenic mice with the alpha4betadelta GABAA (show GABRg1 ELISA Kits) receptor subunit deletion show increased conditioned place preference, but not from delta-deficient or alpha4-deficient knockout mice.
The pathway by which GABRA2 (show GABRA2 ELISA Kits) initially confers risk for eventual alcohol problems begins with a predisposition to sensation-seeking early in adolescence.
Association between premenstrual symptom severity and two genes from the gamma-aminobutyric acid (GABA) pathway: steroid-5-alpha-reductase, alpha polypeptide (show ITGAE ELISA Kits) 1 (show CYP ELISA Kits) (SRD5A1 (show SRD5A1 ELISA Kits)) and gamma-aminobutyric acid receptor subunit alpha-4 (GABRA4).
single nucleotide polymorphisms studied in the GABRA4, GABRE (show GABRE ELISA Kits), and GABRQ (show GABRQ ELISA Kits) genes are not related to the risk for familial ET.
GABRA4 is involved in the etiology of autism and potentially increases autism risk through interaction with GABRB1 (show GABRB1 ELISA Kits).
These results confirmed our earlier findings, indicating GABRA4 and GABRB1 (show GABRB1 ELISA Kits) as genes contributing to autism susceptibility, extending the effect to multiple ethnic groups and suggesting seizures as a stratifying phenotype.
Lower delta mRNA levels in schizophrenia might reflect a reduced number of alpha(1)beta(x)delta (show DLL1 ELISA Kits) GABA(A) receptors that could contribute to deficient tonic inhibition and prefrontal cortical dysfunction in schizophrenia.
Gabra4 KO CD4 (show CD4 ELISA Kits)(+) cells produced increased cytokines.
This study addressed the effects of AW on changes in the expression of Gabra4 and related genes that encode other subunits of GABAARs
GABAA (show GABRg1 ELISA Kits) receptors in the mediodorsal thalamic nucleus (MD) modulate fear extinction.
Increase in GABRA4 activity promotes hippocampal neurogenesis via nuclear factor of activated T cell (show NFATC3 ELISA Kits) (NFATc)4 (show NFATC4 ELISA Kits).
This study demonistrated that alpha4-GABAARs contribute to nRT burst-mediated inhibition and that activity-dependent recruitment of eGABAARs dynamically influences the ventrobasal neuron tonic conductance during nRT tonic spike trains.
Data suggest that the availability of distinct GABA(A) R subtypes (Gabra2, -4, and Gabrd) provides a molecular mechanism endowing spatiotemporal specificity to GABAergic control of neuronal maturation in adult brain.
alpha-4 subunit of the GABAA (show GABRg1 ELISA Kits) receptor is transcriptionally regulated
Gamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the mammalian brain where it acts at GABA-A receptors, which are ligand-gated chloride channels. Chloride conductance of these channels can be modulated by agents such as benzodiazepines that bind to the GABA-A receptor. At least 16 distinct subunits of GABA-A receptors have been identified. This gene encodes subunit alpha-4, which is involved in the etiology of autism and eventually increases autism risk through interaction with another subunit, gamma-aminobutyric acid receptor beta-1 (GABRB1). Alternatively spliced transcript variants encoding different isoforms have been found in this gene.
gamma-aminobutyric acid (GABA) A receptor, alpha 4
, gamma-aminobutyric acid A receptor, alpha 4
, GABA(A) receptor subunit alpha-4
, gamma-aminobutyric acid receptor subunit alpha-4-like
, GABA-A receptor alpha-4 subunit
, gamma-aminobutyric acid (GABA-A) receptor, subunit alpha 4
, gamma-aminobutyric acid receptor subunit alpha-4
, GABA(A) receptor, alpha 4