EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #72702_C
AMPK激活剂
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总览
AICAR是一种腺苷类似物，可选择性激活AMP激活的蛋白激酶（AMPK）。AMPK调节脂类和葡萄糖代谢来维持细胞能量稳态（Hardie and Carling）。
维持与自我更新
·在小鼠胚胎干细胞中诱导多能性网络基因（Klf4、Klf2、 Nanog、 Oct4、 Myc、 Sox2）和表观遗传相关蛋白（Dnmt3a、Mbd3）的上调，并抑制视黄酸诱导的分化(Adamo et al.; Shi et al)。
分化
·促进MC3T3-E1成骨细胞的分化和矿化（Kanazawa et al.）。
·抑制人羊膜间充质干细胞（MSCs）和兔骨髓间充质干细胞（MSCs）的增殖，促进成骨分化，同时抑制成脂分化（Wu et al.）。
·抑制神经干细胞（NSCs）和永生化NSC细胞系C17.2 （C17.2-NSC）的增殖并诱导星形胶质细胞分化（Zang et al. 2008, 2009)。
·在小鼠胚胎干细胞（ES）中降低Nanog表达和细胞增殖，促进红系分化（Chae et al.）。
别名
Acadesine, AICA 核苷；NSC 105823
细胞类型
间充质干/祖细胞，神经干/祖细胞，成骨细胞，多能干细胞
种属
人，小鼠，非人灵长类，其它细胞系，大鼠
应用
分化，培养
研究领域
神经科学，干细胞生物学
CAS 编号
2627-69-2
化学式
C₉H₁₄N₄O₅
分子量
258.2 克/摩尔
纯度
≥98%
通路
AMPK
靶点
AMPK
产品说明书及文档
请在《产品说明书》中查找相关支持信息和使用说明，或浏览下方更多实验方案。
应用领域
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相关材料与文献
技术资料 (2)
文献 (10)
AICAR sustains J1 mouse embryonic stem cell self-renewal and pluripotency by regulating transcription factor and epigenetic modulator expression. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 2013 JAN
Abstract
BACKGROUND/AIMS [corrected] Embryonic stem cells (ES cells) have the capacity to propagate indefinitely, maintain pluripotency, and differentiate into any cell type under defined conditions. As a result, they are considered to be the best model system for research into early embryonic development. AICA ribonucleotide (AICAR) is an activator of AMP-activated protein kinase (AMPK) that is thought to affect ES cell function, but its role in ES cell fate decision is unclear. METHODS In this study, we performed microarray analysis to investigate AICAR downstream targets and further understand its effect on ES cells. RESULTS Our microarray data demonstrated that AICAR can significantly up-regulate pluripotency-associated genes and down-regulate differentiation-associated transcription factors. Although AICAR cannot maintain ES cell identity without LIF, it can antagonize the action of RA-induced differentiation. Using those differentially expressed genes identified, we performed gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis with the Database for Annotation, Visualization and Integrated Discovery (DAVID) online system. AICAR was not only shown to influence the AMPK pathway, but also act on other signaling pathways such as BMP, MAPK and TGF-β, to maintain the stemness of J1 ES cells. Furthermore, AICAR modulated ES cell epigenetic modification by altering the expression of epigenetic-associated proteins, including Dnmt3a, Dnmt3b, Smarca2, Mbd3, and Arid1a, or through regulating the transcription of long intervening non-coding RNA (lincRNA). CONCLUSION Taken together, our work suggests that AICAR is capable of maintaining ES cell self-renewal and pluripotency, which could be useful in future medical treatment.
5-Aminoimidazole-4-carboxyamide ribonucleoside induces G(1)/S arrest and Nanog downregulation via p53 and enhances erythroid differentiation. Stem cells (Dayton, Ohio) 2012 FEB
Abstract
Molecular mechanisms of how energy metabolism affects embryonic stem cell (ESC) pluripotency remain unclear. AMP-activated protein kinase (AMPK), a key regulator for controlling energy metabolism, is activated in response to ATP-exhausting stress. We investigated whether cellular energy homeostasis is associated with maintenance of self-renewal and pluripotency in mouse ESCs (mESCs) by using 5-aminoimidazole-4-carboxyamide ribonucleoside (AICAR) as an activator of AMPK. We demonstrate that AICAR treatment activates the p53/p21 pathway and markedly inhibits proliferation of R1 mESCs by inducing G(1) /S-phase cell cycle arrest, without influencing apoptosis. Treatment with AICAR also significantly reduces pluripotent stem cell markers, Nanog and stage-specific embryonic antigen-1, in the presence of leukemia inhibitory factor, without affecting expression of Oct4. H9 human ESCs also responded to AICAR with induction of p53 activation and repression of Nanog expression. AICAR reduced Nanog mRNA levels in mESCs transiently, an effect not due to expression of miR-134 which can suppress Nanog expression. AICAR induced Nanog degradation, an effect inhibited by MG132, a proteasome inhibitor. Although AICAR reduced embryoid body formation from mESCs, it increased expression levels of erythroid cell lineage markers (Ter119, GATA1, Klf1, Hbb-b, and Hbb-bh1). Although erythroid differentiation was enhanced by AICAR, endothelial lineage populations were remarkably reduced in AICAR-treated cells. Our results suggest that energy metabolism regulated by AMPK activity may control the balance of self-renewal and differentiation of ESCs.
AICAR, a small chemical molecule, primes osteogenic differentiation of adult mesenchymal stem cells. The International journal of artificial organs 2011 DEC
Abstract
The chemical approach to controlling stem cell fates is emerging as a powerful tool, holding great promise in tissue engineering and regenerative medicine. Various small molecules have been demonstrated capable of modulating stem cell differentiation. In this paper, we studied the effects of 5-aminoimidazole-4-carboxamide-1-ß-riboside (AICAR), an activator of AMP-activated protein kinase (AMPK), on mesenchymal stem cells (MSCs). AICAR at high concentrations (1.0-2.0 mM) significantly inhibited proliferation of both human amnion-derived MSCs (hAMSCs) and rabbit bone marrow-derived MSCs (BM-MSCs). Most importantly, AICAR efficiently promoted the osteogenic differentiation of hAMSCs and BM-MSCs in both growth medium and osteogenic medium. However, Metformin, another AMPK activator, showed no such effects. Meanwhile, AICAR significantly inhibited adipogenic differentiation of hAMSCs and BM-MSCs. Our data suggests that AICAR represents a potent molecule, which can be applied in bone tissue regeneration.
更多信息
| Molecular Weight | 258.2 g/mol |
|---|---|
| 种属 | Human, Mouse, Non-Human Primate, Other, Rat |
| Alternative Names | Acadesine; AICA Riboside; NSC 105823 |
| Cas Number | 2627-69-2 |
| Chemical Formula | C₉H₁₄N₄O₅ |
| 纯度 | ≥ 98% |
| Target | AMPK |
| Pathway | AMPK |
