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N-乙酰-L-谷氨酸(NAG)是一种内源性代谢物。1 它是线粒体氨甲酰磷酸合成酶的变构激活剂,该酶参与尿素循环,同时也是细菌中精氨酸生物合成的第一个中间产物。2、3、4 NAG可抑制人肝NAG合成酶(NAGS;Ki=0.25 mM)。5 当浓度为1 mM时,在大鼠脑线粒体制剂中,它还会抑制几种参与线粒体生物能量学的酶,包括异柠檬酸脱氢酶2(IDH2)、线粒体复合体IV(也称为细胞色素c氧化酶)和谷氨酸脱氢酶(GDH)。6 尿中NAG水平升高与编码氨基酰化酶-1(ACY1)的基因突变有关,该酶参与N-乙酰化蛋白的水解。1
Technical Information
CAS Number
1188-37-0
Synonyms
- N-Acetylglutamate
- N-Acetylglutamic Acid
- NAG
Molecular Formula
C7H11NO5
Formula Weight
189.2
Purity
≥90%
Formulation
A solid
Solubility
DMF: 30 mg/mlDMSO: 30 mg/mlEthanol: 5 mg/mlPBS (pH 7.2): 10 mg/ml
SMILES
OC(CC[C@H](NC(C)=O)C(O)=O)=O
InChi Code
InChI=1S/C7H11NO5/c1-4(9)8-5(7(12)13)2-3-6(10)11/h5H,2-3H2,1H3,(H,8,9)(H,10,11)(H,12,13)/t5-/m0/s1
InChi Key
RFMMMVDNIPUKGG-YFKPBYRVSA-N
关键词:- 乙酰谷氨酸激酶
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产品组分
内容
型号
规格 储存温度
乙酰谷氨酸激酶
37359-01 50g
-20 °C
乙酰谷氨酸激酶
37359-02 100g
-20 °C 乙酰谷氨酸激酶
37359-03 250g
-20 °C 操作手册
1 1 常温
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注意事项
保存建议 厂家推荐蓝冰运输。当您收到产品后,按照说明书建议保存于-20°C。 -
FAQ

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Product Description References
1. Sass, J.O., Mohr, V., Olbrich, H., et al. Mutations in ACY1, the gene encoding aminoacylase 1, cause a novel inborn error of metabolism. Am. J. Hum. Genet. 78(3), 401-409 (2006).
2. Alonso, E., and Rubio, V. Binding of N-
acetyl- L- glutamate to rat liver carbamoyl phosphate synthetase (ammonia). Eur. J. Biochem. 135(2), 331-337 (1983). 3. Marshall, M., Metzenberg, R.L., and Cohen, P.P. Physical and kinetic properties of carbamyl phosphate synthetase from frog liver. The Journal of Biological Chemisty 236(8), 2229-2237 (1961).
4. Petri, K., Walter, F.R., Persicke, M., et al. A novel type of N-
acetylglutamate synthase is involved in the first step of arginine biosynthesis in Corynebacterium glutamicum. BMC Genomics 14, 713 (2013). 5. Coudé, F.X., Grimber, G., Parvy, P., et al. N-
Acetyl glutamate synthetase in human liver: Regulation of activity by L- arginine and N- acetylglutamate. Biochem. Biophys. Res. Commun. 102(3), 1016-1020 (1981). 6. Bortoluzzi, V.T., Ribeiro, R.T., Pinheiro, C.V., et al. N-
Acetylglutamate and N- acetylmethionine compromise mitochondrial bioenergetics homeostasis and glutamate oxidation in brain of developing rats: Potential implications for the pathogenesis of ACY1 deficiency. Biochem. Biophys. Res. Commun. 684, 149123 (2023).
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