EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #72222_C
p38 MAPK抑制剂
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总览
SB203580（盐酸盐）是p38 MAPK活性的强效抑制剂（IC₅₀ = 0.6 µM）。它可抑制 p38 MAPK 的α和β同工酶，但不抑制 ERK 或 JNK。（Bain et al., Cuenda et al.）
维持和自我更新
·增强小鼠胚胎干细胞（ES）的生长和自我更新（Qi et al.）。
·促进人 naïve ground state 多能干细胞的长期维持（Gafni et al.）。
·促进人内皮祖细胞的增殖（Seeger et al.）。
·促进新生和成年大鼠心肌细胞的增殖（Seeger et al.）。
分化
·增强人 ES 细胞向心肌细胞的分化（Gaur et al., Graichen et al.）。
·通过抑制早期中胚层来抑制小鼠 ES 细胞向心肌细胞的分化（Davidson and Morange）。
别名
PB 203580，RWJ 64809
细胞类型
心肌细胞，PSC衍生，内皮细胞，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，扩增，培养
研究领域
干细胞生物学
CAS 编号
869185-85-3
化学式
C₂₁H₁₆FN₃OS · HCl
分子量
413.9 g/mol
纯度
≥ 95 %
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
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相关材料与文献
技术资料 (4)
文献 (9)
Hsp25 and the p38 MAPK pathway are involved in differentiation of cardiomyocytes.
Developmental biology 2000 FEB
Abstract
The small heat-shock protein HSP25 is expressed in the heart early during development,and although multiple roles for HSP25 have been proposed,its specific role during development and differentiation is not known. P19 is an embryonal carcinoma cell line which can be induced to differentiate in vitro into either cardiomyocytes or neurons. We have used P19 to examine the role of HSP25 in differentiation. We found that HSP25 expression is strongly increased in P19 cardiomyocytes. Antisense HSP25 expression reduced the extent of cardiomyocyte differentiation and resulted in reduced expression of cardiac actin and the intermediate filament desmin and reduced level of cardiac mRNAs. Thus,HSP25 is necessary for differentiation of P19 into cardiomyocytes. In contrast,P19 neurons did not express HSP25 and antisense HSP25 expression had no effect on neuronal differentiation. The phosphorylation of HSP25 by the p38/SAPK2 pathway is known to be important for certain of its functions. Inhibition of this pathway by the specific inhibitor SB203580 prevented cardiomyocyte differentiation of P19 cells. In contrast,PD90589,which inhibits the ERK1/2 pathway,had no effect. Surprisingly,cardiogenesis was only sensitive to SB203580 during the first 2 days of differentiation,before HSP25 expression increases. In contrast to the effect of antisense HSP25,SB203580 reduced the level of expression of the mesodermal marker Brachyury-T during differentiation. Therefore,we propose that the p38 pathway acts on an essential target during early cardiogenesis. Once this initial step is complete,HSP25 is necessary for the functional differentiation of P19 cardiomyocytes,but its phosphorylation by p38/SAPK2 is not required.
BMP4 supports self-renewal of embryonic stem cells by inhibiting mitogen-activated protein kinase pathways.
Proceedings of the National Academy of Sciences of the United States of America 2004 APR
Abstract
The fate of pluripotent stem cells is tightly controlled during early embryonic development. Both the derivation and the maintenance of embryonic stem cells (ES cells) in vitro depend on feeder cell-derived growth factors that are largely unidentified. To dissect the mechanisms governing pluripotency,we conducted a screen to identify factors that are produced by mouse embryonic fibroblast STO cells and are required to maintain the pluripotency of ES cells. One of the factors is bone morphogenetic protein 4 (BMP4). Unexpectedly,the major effect of BMP4 on the self-renewal of ES cells is accomplished by means of the inhibition of both extracellular receptor kinase (ERK) and p38 mitogen-activated protein kinase (MAPK) pathways,and inhibitors of ERK and p38 MAPKs mimic the effect of BMP4 on ES cells. Importantly,inhibition of the p38 MAPK pathway by SB203580 overcomes the block in deriving ES cells from blastocysts lacking a functional Alk3,the BMP type IA receptor. These results uncover a paradigm for BMP signaling in the biology of pluripotent stem cells.
p38 mitogen-activated protein kinase downregulates endothelial progenitor cells.
Circulation 2005 MAR
Abstract
BACKGROUND Transplantation of endothelial progenitor cells (EPCs) improves neovascularization after ischemia,but patients with coronary artery disease (CAD) or diabetes mellitus show a reduced number of EPCs and impaired functional activity. Therefore,we investigated the effects of risk factors,such as glucose and TNF-alpha,on the number of EPCs in vitro to elucidate the underlying mechanisms. METHODS AND RESULTS EPCs of patients or healthy subjects were isolated from peripheral blood. Incubation with glucose or TNF-alpha dose-dependently reduced the number of EPCs (79.9+/-1.3% and 74.3+/-8.1% of control; Ptextless0.05,respectively). This reduction was not caused by apoptosis. TNF-alpha and glucose induced a dose- and time-dependent activation of the p38 MAP kinase,the downstream kinase mitogen- and stress-activated kinase 1,and the transcription factor cAMP-responsive element-binding protein (CREB),in EPCs. Moreover,EPCs from CAD patients had significantly higher basal p38-phosphorylation levels (1.83+/-0.2-fold increase; Ptextless0.05) compared with healthy subjects. The inhibition of the p38-kinase by SB203580 or infection with a dominant negative p38 kinase adenovirus significantly increased basal number of EPCs (136.7+/-6.3% and 142.9+/-18% versus control,respectively). Likewise,ex vivo cultivation of EPCs from patients with CAD with SB203580 significantly increased the number of EPCs and partially reversed the impaired capacity for neovascularization of EPCs in vivo (relative blood flow: 0.40+/-0.03 versus 0.64+/-0.08,Ptextless0.05). The increased numbers of EPCs by SB203580 were associated with an augmentation of EPC proliferation and a reduction of cells expressing the monocytic marker proteins CD14 and CD64,suggesting that p38 regulates proliferation and differentiation events. CONCLUSIONS These results demonstrate that p38 MAP kinase plays a pivotal role in the signal transduction pathways regulating the number of EPCs ex vivo. SB203580 can prevent the negative effects of TNF-alpha and glucose on the number of EPCs and may be useful to improve the number of EPCs for potential cell therapy.
更多信息
| Molecular Weight | 413.9 g/mol |
|---|---|
| 物种 | 人, 其它物种, 大鼠, 小鼠, 非人灵长类 |
| Alternative Names | PB 203580, RWJ 64809 |
| Cas Number | 869185-85-3 |
| Chemical Formula | C₂₁H₁₆FN₃OS · HCl |
| 纯度 | ≥ 95 % |
| Target | p38 MAPK |
| Pathway | p38 MAPK |
质量保证:
产品仅供研究使用，不用于针对人或动物的诊断或治疗。
产品仅供研究使用，不用于针对人或动物的诊断或治疗。
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