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Merck
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909475

Sigma-Aldrich

5-乙炔基尿苷

≥95%

别名:

5-EU, EU

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About This Item

经验公式（希尔记法）:
C11H12N2O6
CAS号:
69075-42-9
分子量:
268.22
MDL编号:
MFCD00876719
UNSPSC代码:
41106305
NACRES:
NA.22

方案

≥95%

表单

powder

反应适用性

reaction type: click chemistry

储存温度

−20°C

SMILES字符串

[nH]1[c]([n](cc([c]1=O)C#C)[C@@H]2O[C@@H]([C@H]([C@H]2O)O)CO)=O

InChI

1S/C11H12N2O6/c1-2-5-3-13(11(18)12-9(5)17)10-8(16)7(15)6(4-14)19-10/h1,3,6-8,10,14-16H,4H2,(H,12,17,18)/t6-,7-,8-,10-/m1/s1

InChI key

QCWBIPKYTBFWHH-FDDDBJFASA-N

相关类别

应用

这种含炔烃的代谢标记试剂可用于测量增殖细胞中的RNA合成。一旦喂入细胞，该嘧啶核苷就会在活性RNA合成过程中掺入，然后可以使用铜催化的点击反应与荧光染料进行检测。然后可以通过荧光成像、流式细胞仪或高含量成像分析来分析细胞。

储存分类代码

11 - Combustible Solids

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable

历史批次信息供参考:

分析证书(COA)

Lot/Batch Number
MKCV7551
MKCW5208
MKCT7990
MKCV3855
MKCP9643

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Advanced science (Weinheim, Baden-Wurttemberg, Germany), 7(20), 2000157-2000157 (2020-10-27)
Repair of DNA double-strand breaks (DSBs) is essential for genome integrity, and is accompanied by transcriptional repression at the DSB regions. However, the mechanisms how DNA repair induces transcriptional inhibition remain elusive. Here, it is identified that BRD7 participates in
Magdalena P Crossley et al.
Nucleic acids research, 48(14), e84-e84 (2020-06-17)
R-loops are dynamic, co-transcriptional nucleic acid structures that facilitate physiological processes but can also cause DNA damage in certain contexts. Perturbations of transcription or R-loop resolution are expected to change their genomic distribution. Next-generation sequencing approaches to map RNA-DNA hybrids
Xichen Bao et al.
Nature methods, 15(3), 213-220 (2018-02-13)
We combine the labeling of newly transcribed RNAs with 5-ethynyluridine with the characterization of bound proteins. This approach, named capture of the newly transcribed RNA interactome using click chemistry (RICK), systematically captures proteins bound to a wide range of RNAs
Christophe Bourges et al.
EMBO molecular medicine, 12(5), e12112-e12112 (2020-04-03)
Deriving mechanisms of immune-mediated disease from GWAS data remains a formidable challenge, with attempts to identify causal variants being frequently hampered by strong linkage disequilibrium. To determine whether causal variants could be identified from their functional effects, we adapted a
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