EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #72632_C
p38 MAPK抑制剂
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总览
SB202190是一种选择性强、有效、可透过细胞膜的的p38 MAP激酶抑制剂，抑制p38α （SAPK2A、MAPK14）和p38β (SAPK2B、MAPK11)， IC50值分别为50和100 nM (Davies et al.; Jiang et al.)。SB202190作为一种吡啶基咪唑抑制剂，通过与 ATP 结合位点直接结合来抑制 p38 MAP 激酶的活性（Fox et al.）。
维持与自我更新
·提高NPC1缺陷小鼠神经干细胞的自我更新能力（Yang et al.）。
·阻断脂联素介导的造血干细胞增殖（DiMascio et al.）。
·抑制BMP3介导的C3H10T1/2间充质干细胞的增殖（Stewart et al.）。
分化
·诱导人胚胎干细胞分化为心肌细胞（Graichen et al.）。
细胞类型
心肌细胞，PSC衍生，造血干/祖细胞，间充质干/祖细胞，神经干/祖细胞
种属
人，小鼠，非人灵长类，其他物种，大鼠
应用
分化，扩增，培养
研究领域
神经科学，干细胞生物学
CAS 编号
152121-30-7
化学式
C₂₀H₁₄FN₃O
纯度
≥98%
通路
p38 MAPK
靶点
p38 MAPK
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 (3)
文献 (7)
Specificity and mechanism of action of some commonly used protein kinase inhibitors.
The Biochemical journal 2000 OCT
Abstract
The specificities of 28 commercially available compounds reported to be relatively selective inhibitors of particular serine/threonine-specific protein kinases have been examined against a large panel of protein kinases. The compounds KT 5720,Rottlerin and quercetin were found to inhibit many protein kinases,sometimes much more potently than their presumed targets,and conclusions drawn from their use in cell-based experiments are likely to be erroneous. Ro 318220 and related bisindoylmaleimides,as well as H89,HA1077 and Y 27632,were more selective inhibitors,but still inhibited two or more protein kinases with similar potency. LY 294002 was found to inhibit casein kinase-2 with similar potency to phosphoinositide (phosphatidylinositol) 3-kinase. The compounds with the most impressive selectivity profiles were KN62,PD 98059,U0126,PD 184352,rapamycin,wortmannin,SB 203580 and SB 202190. U0126 and PD 184352,like PD 98059,were found to block the mitogen-activated protein kinase (MAPK) cascade in cell-based assays by preventing the activation of MAPK kinase (MKK1),and not by inhibiting MKK1 activity directly. Apart from rapamycin and PD 184352,even the most selective inhibitors affected at least one additional protein kinase. Our results demonstrate that the specificities of protein kinase inhibitors cannot be assessed simply by studying their effect on kinases that are closely related in primary structure. We propose guidelines for the use of protein kinase inhibitors in cell-based assays.
NPC1 gene deficiency leads to lack of neural stem cell self-renewal and abnormal differentiation through activation of p38 mitogen-activated protein kinase signaling.
Stem cells 2006 FEB
Abstract
Neural stem cells (NSCs) are capable of giving rise to neurons,glia,and astrocytes. Although self-renewal and differentiation in NSCs are regulated by many genes,such as Notch and Numb,little is known about the role of defective genes on the self-renewal and differentiation of NSCs from developing brain. The Niemann-Pick type C1 (NPC1) disease is a neurodegenerative disease caused by a mutation of the NPC1 gene that affects the function of the NPC1 protein. The ability of NSC self-renewal and differentiation was investigated using a model of NPC1 disease. The NPC1 disorder significantly affected the self-renewal ability of NSCs,as well as the differentiation. NSCs from NPC1-/- mice showed impaired self-renewal ability compared with the NPC1+/+ mice. These alterations were accompanied by the enhanced activity of p38 mitogen-activated protein kinases (MAPKs). Further,the specific p38 MAPK inhibitor SB202190 improved the self-renewal ability of NSCs from NPC-/- mice. This indicated that the NPC1 deficiency can lead to lack of self-renewal and altered differentiation of NSCs mediated by the activation of p38 MAPK,impairing the generation of neurospheres from NPC1-/- Thus,the NPC1 gene may play a crucial role in NSC self-renewal associated with p38 MAPK.
Identification of Adiponectin as a Novel Hemopoietic Stem Cell Growth Factor
The Journal of Immunology 2007 MAR
Abstract
The hemopoietic microenvironment consists of a diverse repertoire of cells capable of providing signals that influence hemopoietic stem cell function. Although the role of osteoblasts and vascular endothelial cells has recently been characterized,the function of the most abundant cell type in the bone marrow,the adipocyte,is less defined. Given the emergence of a growing number of adipokines,it is possible that these factors may also play a role in regulating hematopoiesis. Here,we investigated the role of adiponectin,a secreted molecule derived from adipocytes,in hemopoietic stem cell (HSC) function. We show that adiponectin is expressed by components of the HSC niche and its receptors AdipoR1 and AdipoR2 are expressed by HSCs. At a functional level,adiponectin influences HSCs by increasing their proliferation,while retaining the cells in a functionally immature state as determined by in vitro and in vivo assays. We also demonstrate that adiponectin signaling is required for optimal HSC proliferation both in vitro and in long term hemopoietic reconstitution in vivo. Finally we show that adiponectin stimulation activates p38 MAPK,and that inhibition of this pathway abrogates adiponectin's proliferative effect on HSCs. These studies collectively identify adiponectin as a novel regulator of HSC function and suggest that it acts through a p38 dependent pathway.
更多信息
| 物种 | 人, 其它物种, 大鼠, 小鼠, 非人灵长类 |
|---|---|
| Cas Number | 152121-30-7 |
| Chemical Formula | C₂₀H₁₄FN₃O |
| 纯度 | ≥ 98% |
| Target | p38 MAPK |
| Pathway | p38 MAPK |
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