5-氮杂胞苷（5-Azacytidine）

总览

5-氮杂胞苷（5-Azacytidine）是核苷胞苷的类似物，可掺入DNA和RNA。5-氮杂胞苷作为一种表观遗传修饰剂，可掺入DNA并与DNA甲基转移酶不可逆结合，从而抑制其活性。

重编程
·通过诱导部分重编程细胞的完全重编程，提高小鼠成纤维细胞向诱导多能干细胞 (iPS) 的重编程效率（Mikkelsen et al.）。
·与曲古抑菌素 A （Trichostatin A）结合，可重置小鼠 iPS 细胞的表观遗传记忆（Kim et al.）。

分化
·促进人类胚胎干细胞向心肌细胞的分化（Yoon et al.）。

癌症研究
·经培养癌细胞测试，显示其具有广泛的抗代谢活性，并且是急性髓性白血病的有效化疗药物。

细胞类型
癌细胞及细胞系，心肌细胞，PSC衍生，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
分化，重编程

研究领域
癌症，干细胞生物学

CAS 编号
320-67-2

化学式
C₈H₁₂N₄O₅

纯度
≥ 95 %

通路
表观遗传学

靶点
DNMT

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Protocols and Documentation

Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.

Document Type

Product Name

Catalog #

Lot #

Language

Document Type

Product Information Sheet

Product Name

5-Azacytidine

Catalog #

72012, 72014

Lot #

All

Language

English

Document Type

Safety Data Sheet

Product Name

5-Azacytidine

Catalog #

72012, 72014

Lot #

All

Language

English

Applications

This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.

Research Area

Workflow Stages

Workflow Stages for Human Pluripotent Stem Cell Research

Reprogramming

Maintenance

Differentiation

Workflow Stages for Mouse Pluripotent Stem Cell Research

Reprogramming

Maintenance

Differentiation

Resources and Publications

Rewriting the epigenetic code for tumor resensitization: a review. Oronsky B et al. Translational oncology 2014 OCT

Abstract

In cancer chemotherapy, one axiom, which has practically solidified into dogma, is that acquired resistance to antitumor agents or regimens, nearly inevitable in all patients with metastatic disease, remains unalterable and irreversible, rendering therapeutic rechallenge futile. However, the introduction of epigenetic therapies, including histone deacetylase inhibitors (HDACis) and DNA methyltransferase inhibitors (DNMTIs), provides oncologists, like computer programmers, with new techniques to overwrite" the modifiable software pattern of gene expression in tumors and challenge the "one and done" treatment prescription. Taking the epigenetic code-as-software analogy a step further�

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Epigenetic memory in induced pluripotent stem cells. Kim K et al. Nature 2010 SEP

Abstract

Somatic cell nuclear transfer and transcription-factor-based reprogramming revert adult cells to an embryonic state, and yield pluripotent stem cells that can generate all tissues. Through different mechanisms and kinetics, these two reprogramming methods reset genomic methylation, an epigenetic modification of DNA that influences gene expression, leading us to hypothesize that the resulting pluripotent stem cells might have different properties. Here we observe that low-passage induced pluripotent stem cells (iPSCs) derived by factor-based reprogramming of adult murine tissues harbour residual DNA methylation signatures characteristic of their somatic tissue of origin, which favours their differentiation along lineages related to the donor cell, while restricting alternative cell fates. Such an 'epigenetic memory' of the donor tissue could be reset by differentiation and serial reprogramming, or by treatment of iPSCs with chromatin-modifying drugs. In contrast, the differentiation and methylation of nuclear-transfer-derived pluripotent stem cells were more similar to classical embryonic stem cells than were iPSCs. Our data indicate that nuclear transfer is more effective at establishing the ground state of pluripotency than factor-based reprogramming, which can leave an epigenetic memory of the tissue of origin that may influence efforts at directed differentiation for applications in disease modelling or treatment.

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Dissecting direct reprogramming through integrative genomic analysis Mikkelsen TS et al. Nature 2008

Abstract

Somatic cells can be reprogrammed to a pluripotent state through the ectopic expression of defined transcription factors. Understanding the mechanism and kinetics of this transformation may shed light on the nature of developmental potency and suggest strategies with improved efficiency or safety. Here we report an integrative genomic analysis of reprogramming of mouse fibroblasts and B lymphocytes. Lineage-committed cells show a complex response to the ectopic expression involving induction of genes downstream of individual reprogramming factors. Fully reprogrammed cells show gene expression and epigenetic states that are highly similar to embryonic stem cells. In contrast, stable partially reprogrammed cell lines show reactivation of a distinctive subset of stem-cell-related genes, incomplete repression of lineage-specifying transcription factors, and DNA hypermethylation at pluripotency-related loci. These observations suggest that some cells may become trapped in partially reprogrammed states owing to incomplete repression of transcription factors, and that DNA de-methylation is an inefficient step in the transition to pluripotency. We demonstrate that RNA inhibition of transcription factors can facilitate reprogramming, and that treatment with DNA methyltransferase inhibitors can improve the overall efficiency of the reprogramming process.

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