EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #72322_C
表观遗传修饰剂；抑制组蛋白 EZH2 赖氨酸甲基转移酶
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总览
Deazaneplanocin A (DZNep) 是一种赖氨酸甲基转移酶抑制剂，尤其针对 EZH2。因此，DZNep 可作为表观遗传修饰剂，通过降低 EZH2 水平，特异性抑制组蛋白 3（赖氨酸 27）的三甲基化。（Miranda et al., Tan et al., Tseng et al.）
重编程
·通过与CHIR99021、Forskolin、Valproic Acid、tranyylcypromine和E-616452联合使用，在重编程后期增加OCT4的表达，使小鼠胚胎成纤维细胞能够进行化学重编程（无需遗传因素），从而分化为诱导多能干细胞 (iPS)（Hou et al.）。
·重新激活人胚胎干细胞中 XIST 依赖的失活 X 染色体（Diaz Perez et al.）。
癌症研究
·抑制多形性胶质母细胞瘤癌症干细胞的自我更新（Suva et al.）。
·与组蛋白去乙酰化酶抑制剂联合使用，抑制急性髓系白血病母细胞的存活（Fiskus et al.）。
细胞类型
癌细胞及细胞系，白血病/淋巴瘤细胞，多能干细胞
种属
人，小鼠，非人灵长类，其它细胞系，大鼠
应用
重编程
研究领域
癌症，干细胞生物学
CAS 编号
102052-95-9
化学式
C₁₂H₁₄N₄O₃
纯度
≥ 97 %
通路
表观遗传学
靶点
组蛋白甲基转移酶
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)
Pluripotent stem cells induced from mouse somatic cells by small-molecule compounds. Science (New York, N.Y.) 2013 AUG
Abstract
Pluripotent stem cells can be induced from somatic cells, providing an unlimited cell resource, with potential for studying disease and use in regenerative medicine. However, genetic manipulation and technically challenging strategies such as nuclear transfer used in reprogramming limit their clinical applications. Here, we show that pluripotent stem cells can be generated from mouse somatic cells at a frequency up to 0.2% using a combination of seven small-molecule compounds. The chemically induced pluripotent stem cells resemble embryonic stem cells in terms of their gene expression profiles, epigenetic status, and potential for differentiation and germline transmission. By using small molecules, exogenous master genes" are dispensable for cell fate reprogramming. This chemical reprogramming strategy has potential use in generating functional desirable cell types for clinical applications."
Derivation of new human embryonic stem cell lines reveals rapid epigenetic progression in vitro that can be prevented by chemical modification of chromatin. Human molecular genetics 2012 FEB
Abstract
Human embryonic stem cells (hESCs) are pluripotent cell types derived from the inner cell mass of human blastocysts. Recent data indicate that the majority of established female XX hESC lines have undergone X chromosome inactivation (XCI) prior to differentiation, and XCI of hESCs can be either XIST-dependent (class II) or XIST-independent (class III). XCI of female hESCs precludes the use of XX hESCs as a cell-based model for examining mechanisms of XCI, and will be a challenge for studying X-linked diseases unless strategies are developed to reactivate the inactive X. In order to recover nuclei with two active X chromosomes (class I), we developed a reprogramming strategy by supplementing hESC media with the small molecules sodium butyrate and 3-deazaneplanocin A (DZNep). Our data demonstrate that successful reprogramming can occur from the XIST-dependent class II nuclear state but not class III nuclear state. To determine whether these small molecules prevent XCI, we derived six new hESC lines under normoxic conditions (UCLA1-UCLA6). We show that class I nuclei are present within the first 20 passages of hESC derivation prior to cryopreservation, and that supplementation with either sodium butyrate or DZNep preserve class I nuclei in the self-renewing state. Together, our data demonstrate that self-renewal and survival of class I nuclei are compatible with normoxic hESC derivation, and that chemical supplementation after derivation provides a strategy to prevent epigenetic progression and retain nuclei with two active X chromosomes in the self-renewing state.
Combined epigenetic therapy with the histone methyltransferase EZH2 inhibitor 3-deazaneplanocin A and the histone deacetylase inhibitor panobinostat against human AML cells. Blood 2009 SEP
Abstract
The polycomb repressive complex (PRC) 2 contains 3 core proteins, EZH2, SUZ12, and EED, in which the SET (suppressor of variegation-enhancer of zeste-trithorax) domain of EZH2 mediates the histone methyltransferase activity. This induces trimethylation of lysine 27 on histone H3, regulates the expression of HOX genes, and promotes proliferation and aggressiveness of neoplastic cells. In this study, we demonstrate that treatment with the S-adenosylhomocysteine hydrolase inhibitor 3-deazaneplanocin A (DZNep) depletes EZH2 levels, and inhibits trimethylation of lysine 27 on histone H3 in the cultured human acute myeloid leukemia (AML) HL-60 and OCI-AML3 cells and in primary AML cells. DZNep treatment induced p16, p21, p27, and FBXO32 while depleting cyclin E and HOXA9 levels. Similar findings were observed after treatment with small interfering RNA to EZH2. In addition, DZNep treatment induced apoptosis in cultured and primary AML cells. Furthermore, compared with treatment with each agent alone, cotreatment with DZNep and the pan-histone deacetylase inhibitor panobinostat caused more depletion of EZH2, induced more apoptosis of AML, but not normal CD34(+) bone marrow progenitor cells, and significantly improved survival of nonobese diabetic/severe combined immunodeficiency mice with HL-60 leukemia. These findings indicate that the combination of DZNep and panobinostat is effective and relatively selective epigenetic therapy against AML cells.
更多信息
| 种属 | Human, Mouse, Non-Human Primate, Other, Rat |
|---|---|
| Cas Number | 102052-95-9 |
| Chemical Formula | C₁₂H₁₄N₄O₃ |
| 纯度 | ≥ 97% |
| Target | Histone Methyltransferase |
| Pathway | Epigenetic |
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