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γ-Aminobutyric acid Sale

(Synonyms: γ-氨基丁酸) 目录号 : GC38010

4-Aminobutyric acid (4-Aminobutanoic acid, GABA, Gamma-aminobutyric acid, Piperidic acid) is a naturally occurring neurotransmitter with central nervous system (CNS) inhibitory activity.

γ-Aminobutyric acid Chemical Structure

Cas No.:56-12-2

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10mM (in 1mL Water)
¥495.00
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100mg
¥450.00
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产品描述

4-Aminobutyric acid (4-Aminobutanoic acid, GABA, Gamma-aminobutyric acid, Piperidic acid) is a naturally occurring neurotransmitter with central nervous system (CNS) inhibitory activity.

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].

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].

[1] Takehara A, et al. Cancer Res. 2007, 67(20):9704-12. [2] Soltani N, et al. Proc Natl Acad Sci U S A. 2011, 108(28):11692-7. [3] Bhat R, et al. Proc Natl Acad Sci U S A. 2010, 107(6):2580-5.

Chemical Properties

Cas No. 56-12-2 SDF
别名 γ-氨基丁酸
Canonical SMILES O=C(O)CCCN
分子式 C4H9NO2 分子量 103.12
溶解度 Water: ≥ 50 mg/mL (484.87 mM) 储存条件 Store at RT
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1 mg 5 mg 10 mg
1 mM 9.6974 mL 48.4872 mL 96.9744 mL
5 mM 1.9395 mL 9.6974 mL 19.3949 mL
10 mM 0.9697 mL 4.8487 mL 9.6974 mL
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