GABA transaminase

GABA transaminase

Valproate-Induced Rodent Model of Autism Spectrum Disorder: Immunogenic Effects and Role of Microglia

Published in Raj Bawa, János Szebeni, Thomas J. Webster, Gerald F. Audette, Immune Aspects of Biopharmaceuticals and Nanomedicines, 2019

Prabha Awale, James C. K. Lai, Srinath Pashikanthi, Alok Bhushan

VPA is a multi-target drug. In addition to those discussed above, other mechanism may also contribute to the ASD-like behavioral deficits induced by VPA. VPA can indirectly inhibit GSK3β and this may alter axonal remodeling in developing neurons [29, 30]. Additionally, since VPA inhibits GABA transaminase, the GABA-metabolizing enzyme but also enhances glutamic acid decarboxylase, the GABA-synthesizing enzyme, VPA could increase the levels of GABA during early development [31]. As GABA plays a critical role in maturation of neuronal networks in the developing brain, alteration in the levels of GABA may lead to disruption of neuronal network and ASD-like behaviors in the offspring.

Screening and identification of novel inhibitors against human 4-aminobutyrate-aminotransferase: A computational approach

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Journal Information

Published in Egyptian Journal of Basic and Applied Sciences, 2018

S. Vijayakumar, G. Kasthuri, S. Prabhu, P. Manogar, N. Parameswari

4-aminobutyrate aminotransferase (GABA) receptors are the key mediators of fast inhibitory synaptic transmission in the central nervous system of mammals [1]. Its dreadful conditions become involved in catalysis by aminobutyrate transaminase (ABAT, GABA transaminase) for the period of the early stage [2]. It is divided into the three kinds of receptors namely GABAA, GABAB, and GABAC [3[4][5][6]–7] . These are all mainly affected by the mutations of GABA subunit genes from the nervous system.

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Valproate-Induced Rodent Model of Autism Spectrum Disorder: Immunogenic Effects and Role of Microglia

Screening and identification of novel inhibitors against human 4-aminobutyrate-aminotransferase: A computational approach