EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #72702_C
AMPK激活剂
若您需要咨询产品或有任何技术问题，请通过官方电话 400 885 9050 或邮箱 info.cn@stemcell.com 与我们联系。
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，其他物种，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 g/mol
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
本产品专为以下研究领域设计，适用于工作流程中的高亮阶段。探索这些工作流程，了解更多我们为各研究领域提供的其他配套产品。
相关材料与文献
技术资料 (2)
文献 (10)
5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) inhibits insulin-stimulated glucose transport in 3T3-L1 adipocytes.
Diabetes 2000 OCT
Abstract
Incubation of skeletal muscle with 5-aminoimidazole-4carboxamide ribonucleoside (AICAR),a compound that activates 5'-AMP-activated protein kinase (AMPK),has been demonstrated to stimulate glucose transport and GLUT4 translocation to the plasma membrane. In this study,we characterized the AMPK cascade in 3T3-L1 adipocytes and the response of glucose transport to incubation with AICAR. Both isoforms of the catalytic alpha-subunit of AMPK are expressed in 3T3-L1 adipocytes,in which AICAR stimulated AMPK activity in a time- and dose-dependent fashion. AICAR stimulated 2-deoxy-D-glucose transport twofold and reduced insulin-stimulated uptake to 62% of the control transport rate dose-dependently,closely correlating with the activation of AMPK. AICAR also inhibited insulin-stimulated GLUT4 translocation,assessed using the plasma membrane lawn assay. The effects of AICAR on insulin-stimulated glucose transport are not mediated by either adenosine receptors or nitric oxide synthase and are mediated downstream of phosphatidylinositol 3'-kinase stimulation. We propose that in contrast to skeletal muscle,in which AMPK stimulation promotes glucose transport to provide ATP as a fuel,AMPK stimulation inhibits insulin-stimulated glucose transport in adipocytes,inhibiting triacylglycerol synthesis,to conserve ATP under conditions of cellular stress. Investigation of the mode of action of AICAR and AMPK may,therefore,give insight into the mechanism of insulin action.
Adiponectin and AMP kinase activator stimulate proliferation, differentiation, and mineralization of osteoblastic MC3T3-E1 cells.
BMC cell biology 2007 JAN
Abstract
BACKGROUND Adiponectin is a key mediator of the metabolic syndrome that is caused by visceral fat accumulation. Adiponectin and its receptors are known to be expressed in osteoblasts,but their actions with regard to bone metabolism are still unclear. In this study,we investigated the effects of adiponectin on the proliferation,differentiation,and mineralization of osteoblastic MC3T3-E1 cells. RESULTS Adiponectin receptor type 1 (AdipoR1) mRNA was detected in the cells by RT-PCR. The adenosine monophosphate-activated protein kinase (AMP kinase) was phosphorylated by both adiponectin and a pharmacological AMP kinase activator,5-amino-imidazole-4-carboxamide-riboside (AICAR),in the cells. AdipoR1 small interfering RNA (siRNA) transfection potently knocked down the receptor mRNA,and the effect of this knockdown persisted for as long as 10 days after the transfection. The transfected cells showed decreased expressions of type I collagen and osteocalcin mRNA,as determined by real-time PCR,and reduced ALP activity and mineralization,as determined by von Kossa and Alizarin red stainings. In contrast,AMP kinase activation by AICAR (0.01-0.5 mM) in wild-type MC3T3-E1 cells augmented their proliferation,differentiation,and mineralization. BrdU assay showed that the addition of adiponectin (0.01-1.0 mug/ml) also promoted their proliferation. Osterix,but not Runx-2,appeared to be involved in these processes because AdipoR1 siRNA transfection and AICAR treatments suppressed and enhanced osterix mRNA expression,respectively. CONCLUSION Taken together,this study suggests that adiponectin stimulates the proliferation,differentiation,and mineralization of osteoblasts via the AdipoR1 and AMP kinase signaling pathways in autocrine and/or paracrine fashions.
AICAR induces astroglial differentiation of neural stem cells via activating the JAK/STAT3 pathway independently of AMP-activated protein kinase.
The Journal of biological chemistry 2008 MAR
Abstract
Neural stem cell differentiation and the determination of lineage decision between neuronal and glial fates have important implications in the study of developmental,pathological,and regenerative processes. Although small molecule chemicals with the ability to control neural stem cell fate are considered extremely useful tools in this field,few were reported. AICAR is an adenosine analog and extensively used to activate AMP-activated protein kinase (AMPK),a metabolic fuel gauge" of the biological system. In the present study�
更多信息
| Molecular Weight | 258.2 g/mol |
|---|---|
| 物种 | 人, 其它物种, 大鼠, 小鼠, 非人灵长类 |
| Alternative Names | Acadesine; AICA Riboside; NSC 105823 |
| Cas Number | 2627-69-2 |
| Chemical Formula | C₉H₁₄N₄O₅ |
| 纯度 | ≥ 98% |
| Target | AMPK |
| Pathway | AMPK |
沪公网安备31010102008431号
在线联系