EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #72062_C
p53抑制剂
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总览
环状Pifthrin-Alpha是一种可渗透细胞且可逆的p53介导的细胞凋亡和p53依赖性基因转录抑制剂。它是非环状Pifithrin-Alpha的更稳定且细胞毒性更低的类似物。据报道，环状Pifithrin-Alpha还可激活芳烃受体（Fernandez-Cruz et al., Gary & Jensen, Komarov et al.）。
重编程
·提高小鼠胚胎成纤维细胞重编程为诱导多能干细胞的效率（Liao et al.）。
维持和自我更新
·降低紫外线诱导的小鼠胚胎干细胞凋亡（Qin et al.）。
·增加小鼠体内和体外造血干细胞和祖细胞的数量，并降低辐射诱导的这些细胞死亡（Leonova et al.）。
别名
环状PFT-α，环状Pifithrin-α，PFT-β，Pifithrin-β
细胞类型
造血干/祖细胞，多能干细胞
种属
人，小鼠，非人灵长类，其它细胞系，大鼠
应用
扩增，培养，重编程
研究领域
干细胞生物学
CAS 编号
511296-88-1
化学式
C₁₆H₁₆N₂S · HBr
分子量
349.3 克/摩尔
纯度
≥ 95 %
通路
p53
靶点
p53
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 (3)
文献 (6)
Inhibition of PTEN tumor suppressor promotes the generation of induced pluripotent stem cells. Molecular therapy : the journal of the American Society of Gene Therapy 2013 JUN
Abstract
Induced pluripotent stem cells (iPSCs) can be generated from patients with specific diseases by the transduction of reprogramming factors and can be useful as a cell source for cell transplantation therapy for various diseases with impaired organs. However, the low efficiency of iPSC derived from somatic cells (0.01-0.1%) is one of the major problems in the field. The phosphoinositide 3-kinase (PI3K) pathway is thought to be important for self-renewal, proliferation, and maintenance of embryonic stem cells (ESCs), but the contribution of this pathway or its well-known negative regulator, phosphatase, and tensin homolog deleted on chromosome ten (Pten), to somatic cell reprogramming remains largely unknown. Here, we show that activation of the PI3K pathway by the Pten inhibitor, dipotassium bisperoxo(5-hydroxypyridine-2-carboxyl)oxovanadate, improves the efficiency of germline-competent iPSC derivation from mouse somatic cells. This simple method provides a new approach for efficient generation of iPSCs.
Biological and chemical studies on aryl hydrocarbon receptor induction by the p53 inhibitor pifithrin-α and its condensation product pifithrin-β. Life sciences 2011 APR
Abstract
AIMS Pifithrin α (PFTα), an inhibitor of the p53 protein, is regarded as a lead compound for cancer and neurodegenerative disease therapy. There is some evidence that this compound activates the aryl hydrocarbon receptor (AhR) in a complete independent way of the p53 inhibition and that it is easily converted to its condensation product pifithrin β (PFTβ). The aim of this study was to explore the ability of PFTα and of PFTβ to induce a variety of AhR mediated processes. MAIN METHODS Computational analysis using quantum chemical calculations and chemical analysis have been used to study the conformation of the compounds as well as the cyclization reaction. The AhR mediated processes of these compounds have been studied in a rainbow trout cell line (RTG-2) and in a rat hepatoma cell line (H4IIE). KEY FINDINGS PFTα molecule could not take a planar conformation required for AhR activation whereas PFTβ showed a conformation similar to those of the prototypical AhR ligand β-naphthoflavone. In both cell lines, PFTα and PFTβ provoked different responses related with AhR activation. However, when cyclization of PFTα to PFTβ was hampered by acetylation of the exocyclic nitrogen, all these responses were not observed. These results lead to the conclusion that the activation of the AhR is probably caused by PFTβ instead of PFTα. SIGNIFICANCE Since PFTα is a promising compound for the development of new pharmaceuticals inhibiting p53, the chemical instability of this compound as well as the capacity of its transformation product should be taken into account.
A small molecule inhibitor of p53 stimulates amplification of hematopoietic stem cells but does not promote tumor development in mice. Cell cycle (Georgetown, Tex.) 2010 APR
Abstract
It has been shown that genetic inhibition of p53 leads to enhanced proliferation of hematopoietic stem cells (HSCs). This could, in theory, contribute to the increased frequency of tumor development observed in p53-deficient mice and humans. In our previous work, we identified chemical p53 inhibitors (PFTs) that suppress the transactivation function of p53 and protect cultured cells and mice from death induced by gamma irradiation (IR). Here we found that when applied to bone marrow cells in vitro or injected into mice, PFTb impeded IR-induced reduction of hematopoietic stem cell (HSC) and hematopoietic progenitor cell (HPC) population sizes. In addition, we showed that PFTb stimulated HSC and HPC proliferation in the absence of IR in vitro and in vivo and mobilized HSCs to the peripheral blood. Importantly, however, PFTb treatment did not affect the timing or frequency of tumor development in irradiated p53 heterozygous mice used as a model for determination of carcinogenicity. Thus, although PFTb administration led to increased numbers of HSCs and HPCs, it was not carcinogenic in mice. These findings suggest that chemical p53 inhibitors may be clinically useful as safe and effective stimulators of hematopoiesis.
更多信息
| Molecular Weight | 349.3 g/mol |
|---|---|
| 种属 | Human, Mouse, Non-Human Primate, Other, Rat |
| Alternative Names | Cyclic PFT-α, Cyclic Pifithrin-α, PFT-β, Pifithrin-β |
| Cas Number | 511296-88-1 |
| Chemical Formula | C₁₆H₁₆N₂S · HBr |
| 纯度 | ≥ 95% |
| Target | p53 |
| Pathway | p53 |
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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。
