IA06801 阿扎胞苷(10mM in DMSO,无菌) 表观遗传学 索莱宝

IA06801 阿扎胞苷(10mM in DMSO,无菌)

表观遗传学 索莱宝
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  • ¥200 - 650
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  • 北京
  • IA06801
  • 2025年07月23日
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    • 详细信息
    • 技术资料
    • 保存条件

      Stroe at -20℃,6 months.

    • 保质期

      Stroe at -20℃,6 months.

    • 英文名

      5-Azacytidine(10mM in DMSO,Sterile)

    • 库存

      现询

    • 供应商

      北京索莱宝科技有限公司

    • CAS号

      320-67-2

    • 规格

      0.1ml/0.3ml/0.5ml/1.5ml/1ml

    规格:0.1ml产品价格:¥200.0
    规格:0.3ml产品价格:¥300.0
    规格:0.5ml产品价格:¥400.0
    规格:1.5ml产品价格:¥650.0
    规格:1ml产品价格:¥500.0

    基本信息
    CASNo.320-67-2
    中文名称阿扎胞苷(10mM in DMSO,无菌)
    英文名称5-Azacytidine(10mM in DMSO,Sterile)
    分子式C8H12N4O5
    分子量244.2
    溶解性请根据自己的实验要求使用。
    外观(性状)无菌溶液
    储存条件Stroe at -20℃,6 months.
    靶点DNA Methyltransferase;Autophagy
    通路Epigenetics;Autophagy
    背景说明5-Azacytidine是一种胞苷核苷类似物,也是一种DNA 甲基化抑制剂,通过与 DNA 结合共价捕获 DNA甲基转移酶 (DNA methyltransferases)特异性抑制DNA甲基化。5-Azacytidine 通过降低 DNA 甲基化水平调节基因表达。
    生物活性5-Azacytidine (Azacitidine; 5-AzaC; Ladakamycin) is a nucleoside analogue of cytidine that specifically inhibits DNA methylation. 5-Azacytidine is incorporated into DNA to covalently trap DNA methyltransferases and contributes to reverse epigenetic changes. 5-Azacytidine induces cell autophagy.[1-4]
    In Vitro5-Azacytidine was first synthesized almost 40 years ago. It was demonstrated to have a wide range of anti-metabolic activities when tested against cultured cancer cells and to be an effective chemotherapeutic agent for acute myelogenous leukemia.The finding that 5-azacytidine was incorporated into DNA and that, when present in DNA, it inhibited DNA methylation, led to widespread use of 5-azacytidine and 5-aza-2-deoxycytidine (Decitabine) to demonstrate the correlation between loss of methylation in specific gene regions and activation of the associated genes. [1]
    细胞实验Twenty mL of cells (circa 1×104 cells/mL) are pipetted into sterilized culture tubes with screw caps and incubated at 37°C overnight. The experiment is initiated by the addition of 1 mL of 5-Azacytidine (5-azaCR) or medium for a given period (from 0 to 240 min) prior to the addition of 1 mL of metabolite (or medium). Cell growth is determined twice a day for 3 days by means of a Model A Coulter counter. To determine IDSO and ID90 values, 5 mL of L1210 cells (5×103 cells/mL) are incubated with the drug at 37°C for 3 days, and cell growth is determined.[3]
    动物实验For the in vivo experiments, leukemic mice (bearing circa 1×103 cells/animal) are given injections i.p. with 0.2 mL of 5-Azacytidine (5-azaCR) of a given concentration. Two hr later, the reaction is started by injecting 0.5 mL of labeled metabolite (TdR-3H or UR-3H, 10 /μCi/12.5 μg). After 1 hr, animals (3 mice/group) are killed by cervical fracture.[3]
    激酶实验A crude cell-free extract is isolated from LI 210 cells in culture by suspension of the cells in a given volume of 0.05mol/LTris-HCl buffer, pH 7.4, and sonic extraction with a Biosonik at 70% maximal output for 30 sec. The supernatant is collected after centrifugation at 105,000 × g for 60 min (4°C) in a Model L Spinco ultracentrifuge. The final protein concentration of the cell-free extracts is approximately 3 mg/mL. The extracts are used as the source of enzymes. Ribonucleotide reductase activity is measured. A unit of enzyme is defined as the amount that catalyzed dCMP synthesis at a rate of 1 mμmole/hr. The assay systems for the measurement of pyrimidine nucleoside (CR) and deoxynucleoside (TdR, CdR) kinases are essentially those described by Chu and Fischer. However, reactions are terminated by heating for 2 min in a boiling water bath, and the phosphorylated derivatives are isolated according to the method of Bach. Fifty-jul aliquots are applied to 1-inch discs of diethylaminoethyl paper, which are then placed in counting vials and eluted with 0.5 mL of 0.5 mol/LPCA. After 1 hr, 12 mL of Diotol are added, and the radioactivity is determined.[3]
    数据来源文献[1]. Christman JK. 5-Azacytidine and 5-aza-2-deoxycytidine as inhibitors of DNA methylation: mechanistic studies and their implications for cancer therapy. Oncogene. 2002 Aug 12;21(35):5483-95.
    [2]. Creusot F, et al. Inhibition of DNA methyltransferase and induction of Friend erythroleukemia cell differentiation by 5-azacytidineand 5-aza-2-deoxycytidine. J Biol Chem. 1982 Feb 25;257(4):2041-8.
    [3]. Li LH,et al. Cytotoxicity and mode of action of 5-azacytidine on L1210 leukemia. Cancer Res. 1970 Nov;30(11):2760-9.
    [4]. Marycz K, et al. 5-Azacytidine?and?Resveratrol?Enhance?Chondrogenic?Differentiation?of?Metabolic?Syndrome-Derived?Mesenchymal?Stem?Cells?by?Modulating?Autophagy.Oxid Med Cell Longev.?2019 May 12;2019:1523140.
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