Transcriptional control ofGad2

Abstract

Gad2 encodes GAD65, which is present preferentially in presynaptic terminals for synthesis of GABA for vesicle release. Gad2 is a regulatory target of cell activities in various brain functions and in GABA perturbation-related neurological diseases. However, our understanding of how Gad2 is transcriptionally regulated and how Gad2 transcription responds to changing cell environment under these conditions is still limited. This review discusses recent advances in the regulatory mechanisms for Gad2 transcription and highlights the characteristics of TATA-less Gad2 promoters and regulation of Gad2 transcription by CREB and by activity-dependent epigenetic modification of the chromatin structure in regulatory elements of the Gad2 gene.

Role of GAD2 and HTR1B genes in early‐onset obsessive‐compulsive disorder: results from transmission disequilibrium study

“…This is in accordance with differences in GABA neurotransmission between males and females (Simpson et al ). The dynamic expression of GAD2 required a complex regulation of its transcription (Pan ), which seems to be under control of estrogen receptors (Hudgens et al ) and could be modulated by sex steroids (Noriega et al ).…”

The role of glutamate decarboxylase 65 in gastric cancer development, progression, and prognosis

“…γ‐Aminobutyric acid (GABA) is the predominant and most ubiquitous inhibitory neurotransmitter in the mammalian central nervous system. Once released from synaptic terminals, GABA inhibits the activities of target cells by opening inhibitory ion channels on postsynaptic membranes, providing general inhibition of mature neurons in the brain and spinal cord . GABA is synthesized from glutamate by two isoforms of the rate‐limiting enzyme glutamate decarboxylase (GAD): GAD67 and GAD65.…”

“…GABA is synthesized from glutamate by two isoforms of the rate‐limiting enzyme glutamate decarboxylase (GAD): GAD67 and GAD65. The two isoforms are encoded, respectively, by two separate genes, GAD1 and GAD2 , which originated from the ancient duplication of a single ancestral form during vertebrate evolution . Accumulating evidence indicates that GABA and GAD play important roles in cancer progression …”

“…Once released from synaptic terminals, GABA inhibits the activities of target cells by opening inhibitory ion channels on postsynaptic membranes, providing general inhibition of mature neurons in the brain and spinal cord. [1][2][3][4] GABA is synthesized from glutamate by two isoforms of the rate-limiting enzyme glutamate decarboxylase (GAD): GAD67 and GAD65. The two isoforms are encoded, respectively, by two separate genes, GAD1 and GAD2, which originated from the ancient duplication of a single ancestral form during vertebrate evolution.…”

“…The two isoforms are encoded, respectively, by two separate genes, GAD1 and GAD2, which originated from the ancient duplication of a single ancestral form during vertebrate evolution. [1][2][3][4] Accumulating evidence indicates that GABA and GAD play important roles in cancer progression. [5][6][7][8][9] Al-Wadei et al found that social stress promotes tumour growth and GABA inhibits tumour growth in mouse models of non-small-cell lung cancer.…”