3031-95-6
基本信息
Succino-AICAR
5-Aminoimidazole-4-N-succinocarboxamide ribonucleotide
5'-Phosphoribosyl-4-(N-succinocarboxamide)-5-aminoimidazole
N-Succinyl-5-aMinoiMidazole-4-carboxaMide Ribose 5'-Phosphate
N-[[5-Amino-1-(5-O-phosphono-β-D-ribofuranosyl)-1H-imidazol-4-yl]carbonyl]-L-aspartic acid
N-[[5-Amino-1-(5-O-phosphono-b-D-ribofuranosyl)-1H-imidazoL-4-yl]carbonyl]-L-aspartic acid
L-Aspartic acid, N-[[5-amino-1-(5-O-phosphono-β-D-ribofuranosyl)-1H-imidazol-4-yl]carbonyl]-
2-[[1-(5-O-Phosphono-β-D-ribofuranosyl)-5-amino-1H-imidazol]-4-ylcarbonylamino]succinic acid
(2S)-2-[[5-amino-1-[(2R,3R,4S,5R)-3,4-dihydroxy-5-(phosphonooxymethyl)oxolan-2-yl]imidazole-4-carbonyl]amino]butanedioic acid
物理化学性质
| 熔点 | >189°C (dec.) |
| 密度 | 2.18±0.1 g/cm3(Predicted) |
| 储存条件 | Hygroscopic, -20°C Freezer, Under inert atmosphere |
| 溶解度 | 少许溶于甲醇和水 |
| 酸度系数(pKa) | 1.86±0.10(Predicted) |
| 形态 | 固体 |
| 颜色 | 白色至灰白色 |
常见问题列表
N-琥珀酰基-5-氨基咪唑-4-羧酰胺5'-磷酸核糖是嘌呤代谢产物。 由于腺苷是神经元功能的有效抑制剂，可抑制几种兴奋递质的释放并引发神经元的直接过级化，因此腺苷琥珀酸裂合酶（ASase）缺乏症患者出现的症状可能反映了琥珀酰嘌呤对神经传递的干扰。
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Human Endogenous Metabolite
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SAICAR accumulation induces nuclear localization of PKM2. PKM2-SAICAR phosphorylates and activates Erk1/2, which in turn sensitizes PKM2 for SAICAR binding through phosphorylation. Additionally, PKM2-SAICAR was necessary to induce sustained Erk1/2 activation and mitogen-induced cell proliferation. SAICAR-PKM2 interaction is necessary and sufficient to induce H3 T11 and Erk1/2 phosphorylation.
Upon glucose starvation, cellular SAICAR concentration increases in an oscillatory manner and stimulates PKM2 activity in cancer cells. The SAICAR-PKM2 interaction also promotes cancer cell survival in glucose-limited conditions. In glucose-limited conditions, cells with higher SAICAR concentrations (
adsl-kd
cells or cells overexpressing PAICS) survive better while
paics-kd
cells died earlier than control-kd cells. SAICAR promotes cancer cell survival in glucose-limited conditions.