4-Aminobutyric acid (GABA)

製品コードS4700 バッチS470002

印刷

化学情報

Chemical Structure Synonyms 4-Aminobutanoic acid, GABA, Gamma-aminobutyric acid, Piperidic acid Storage
(From the date of receipt)		 3 years -20°C powder
1 years -80°C in solvent
化学式

C4H9NO2
分子量 103.12 CAS No. 56-12-2
Solubility (25°C)* 体外 Water 21 mg/mL (203.64 mM)
DMSO Insoluble
Ethanol Insoluble
* <1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

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生物活性

製品説明 4-Aminobutyric acid (4-Aminobutanoic acid, GABA, Gamma-aminobutyric acid, Piperidic acid) is a naturally occurring neurotransmitter with central nervous system (CNS) inhibitory activity.
in vitro γ-Aminobutyric acid (GABA) functions primarily as an inhibitory neurotransmitter in the mature central nervous system. The addition of GABA into the cell culture medium promoted the proliferation of GABRP-expressing PDAC cells, but not GABRP-negative cells, and GABAA receptor antagonists inhibited this growth-promoting effect by GABA. The HEK293 cells constitutively expressing exogenous GABRP revealed the growth-promoting effect of GABA treatment. GABA treatment in GABRP-positive cells increased intracellular Ca2+ levels and activated the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/Erk) cascade[1]. GABA exerts antidiabetic effects by acting on both the islet β-cells and immune system. Unlike in adult brain or islet α-cells in which GABA exerts hyperpolarizing effects, in islet β-cells, GABA produces membrane depolarization and Ca2+ influx, leading to the activation of PI3K/Akt-dependent growth and survival pathways[2].
in vivo GABA is the principal inhibitory neurotransmitter in the adult brain that has a parallel inhibitory role in the immune system. GABAergic medications are used to treat anxiety, alcohol withdrawal, epilepsy, and to induce sedation, and anesthesia. GABA is neuroprotective in animal models of stroke. GABA treatment decreases inflammatory cytokine production in peripheral macrophages. It decreases T cell autoimmunity and the development of inflammatory responses in the nonobese diabetic mouse model of type 1 diabetes[3]. In the adult brain, GABA induces a fast inhibition in neurons mainly through the GABAA receptor (GABAAR). GABA is produced by pancreatic β-cells. GABA released from β-cells can act on GABAAR in the α-cells, causing membrane hyperpolarization and hence suppressing glucagon secretion. GABA-treated mice showed higher circulating insulin, lower glucagon, nearly normal glycemia, improved metabolic conditions, and maintained close to normal glucose tolerance during a period of 53 d after STZ injections[2].

プロトコル(参考用のみ)

細胞アッセイ 細胞株 PDAC cell lines KLM-1, SUIT-2, KP-1N, PK-1, PK-45P, and PK-59
濃度 0, 1, 10, 100 μmol/L
反応時間 6 days
実験の流れ GABRP-positive cell lines, KLM-1 and PK-45P, and GABRP-negative cell lines, PK-59 and KP-1N, are incubated with GABA or GABA receptor agonist Muscimol at serial concentration (0, 1, 10, 100 μmol/L) in appropriate medium supplemented with 1% FBS for 6 days. To inhibit the GABA-mediated pathway, cells are incubated with 250 μmol/L of GABAA receptor antagonist bicuculline methiodide or 1 mmol/L of GABAB receptor antagonist CGP-35348. After 6 days of exposure to either of these drugs, cell viability is measured by MTT assay as described above.
動物実験 動物モデル Mice(CD1 mice) with STZ-induced diabetes
投薬量 20 μmol per mouse
投与方法 i.p.

Selleckの高級品が、幾つかの出版された研究調査結果（以下を含む）で使われた：

The delta subunit of the GABAA receptor is necessary for the GPT2-promoted breast cancer metastasis [ Theranostics, 2023, 13(4):1355-1369] PubMed: 36923530

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人間や獣医の診断であるか治療的な使用のためにでない。

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