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Chemical Compound Review

Aminalon     4-aminobutanoic acid

Synonyms: Gammalon, Aminalone, GABA, Aminobutyric acid, Aminobutyric Acids, ...
 
 
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Disease relevance of Aminobutyric acid

 

Psychiatry related information on Aminobutyric acid

 

High impact information on Aminobutyric acid

  • Three molecularly distinct Cl- channel families (CLC, CFTR, and ligand-gated GABA and glycine receptors) are well established [12].
  • Molecular biology entered the field of mammalian amino acid transporters in 1990-1991 with the cloning of the first GABA and cationic amino acid transporters [13].
  • Surprisingly, neurexin also induces GABA postsynaptic differentiation [14].
  • We report that an Ala322Asp mutation in GABRA1, encoding the alpha1 subunit of the gamma-aminobutyric acid receptor subtype A (GABA(A)), is found in affected individuals of a large French Canadian family with juvenile myoclonic epilepsy [15].
  • These mice also showed aberrant migration and differentiation of interneurons containing gamma-aminobutyric acid (GABAergic interneurons) in the ganglionic eminence and neocortex as well as abnormal testicular differentiation [16].
 

Chemical compound and disease context of Aminobutyric acid

 

Biological context of Aminobutyric acid

 

Anatomical context of Aminobutyric acid

 

Associations of Aminobutyric acid with other chemical compounds

 

Gene context of Aminobutyric acid

  • We report a 50-60 kb domain of allele-specific replication between the gamma-aminobutyric acid receptor subunit beta 3 (GABRB3) and alpha 5 (GABRA5) genes [36].
  • Studies in the nematode Caenorhabditis elegans have implicated the gene unc-47 in the release of GABA [25].
  • The gene unc-25 is necessary for GABA expression and probably encodes the GABA biosynthetic enzyme glutamic acid decarboxylase [37].
  • We also show that the Nf1(+/-) mice have increased GABA (gamma-amino butyric acid)-mediated inhibition and specific deficits in long-term potentiation, both of which can be reversed by decreasing Ras function [38].
  • In unc-30 mutants the D neurons lack GABA and have defects in axonal pathfinding and synaptic connections (J. White, personal communication) [39].
  • Since intracellular GABA levels are modulated by neuronal activity, our results implicate GAD67-mediated GABA synthesis in activity-dependent regulation of inhibitory innervation patterns [40].
  • As a consequence of the mutation, her1 plants accumulate high GABA levels in all their organs [41].
 

Analytical, diagnostic and therapeutic context of Aminobutyric acid

References

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