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Merck
CN

D1916

5,6-二氯苯并咪唑 1-β-D-核苷

≥98% (HPLC), powder, RNA synthesis inhibitor

别名:

5,6-二氯-1-β-D-呋喃基苯并咪唑, 5,6-二氯苯并咪唑核糖苷, DRB

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关于此项目

经验公式(希尔记法):
C12H12Cl2N2O4
化学文摘社编号:
分子量:
319.14
UNSPSC Code:
12352200
eCl@ss:
32151902
PubChem Substance ID:
NACRES:
NA.77
Beilstein/REAXYS Number:
39123
MDL number:
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产品名称

5,6-二氯苯并咪唑 1-β-D-核苷,

SMILES string

OC[C@H]1O[C@H]([C@H](O)[C@@H]1O)n2cnc3cc(Cl)c(Cl)cc23

InChI

1S/C12H12Cl2N2O4/c13-5-1-7-8(2-6(5)14)16(4-15-7)12-11(19)10(18)9(3-17)20-12/h1-2,4,9-12,17-19H,3H2/t9-,10-,11-,12-/m1/s1

InChI key

XHSQDZXAVJRBMX-DDHJBXDOSA-N

form

powder

storage temp.

−20°C

Quality Level

Gene Information

Application

5,6-二氯苯并咪唑1-β-D-呋喃核苷用作:
  • 抑制剂,抑制小鼠黑色素瘤细胞RNA聚合酶II
  • 抑制人前列腺上皮细胞系细胞周期蛋白 D1 mRNA合成
  • 抑制Jurkat细胞白介素-2基因转录

Biochem/physiol Actions

5,6-二氯苯并咪唑1-β-D-呋喃核苷(DRB),一种核苷类似物,可通过磷酸化 RNA聚合酶II C端结构域,使其失活,停止mRNA合成 还能干扰DNA拓扑异构酶II,能调节对细胞因子的应答,通过RNA修饰阻断人免疫缺陷病毒(HIV)。它还抑制细胞周期蛋白依赖性激酶(CDK)7和9,促进白血病细胞凋亡。可作为治疗剂治疗癌症。
RNA合成抑制剂;可导致转录提前终止。 CK2(酪蛋白激酶-2)抑制剂。

Features and Benefits

该化合物是基因调控研究的推荐产品。点击这里 发现更多精选基因调控产品。了解更多有关用于其他研究领域的生物活性小分子的信息,请访问 sigma.com/discover-bsm

存储类别

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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Synthesis and biological evaluation of new 5, 6-dichlorobenzimidazole nucleoside derivatives
Gosselin G, et al.
Antiviral Chemistry & Chemotherapy, 5(4), 243-256 (1994)
The cyclin-dependent kinase inhibitor 5, 6-dichloro-1-beta-D-ribofuranosylbenzimidazole induces nongenotoxic, DNA replication-independent apoptosis of normal and leukemic cells, regardless of their p53 status
Turinetto V, et al.
BMC Cancer, 9(1), 281-281 (2009)
Lisa Fish et al.
Genes & development, 30(4), 386-398 (2016-02-18)
Post-transcriptional deregulation is a defining feature of metastatic cancer. While many microRNAs have been implicated as regulators of metastatic progression, less is known about the roles and mechanisms of RNA-binding proteins in this process. We identified muscleblind-like 1 (MBNL1), a
M Ljungman et al.
Oncogene, 18(3), 583-592 (1999-02-16)
The mechanisms by which the p53 response is triggered following exposure to DNA-damaging agents have not yet been clearly elucidated. We and others have previously suggested that blockage of RNA polymerase II may be the trigger for induction of the
Transcriptional regulation of interleukin-2 gene expression is impaired by copper deficiency in Jurkat human T lymphocytes
Hopkins RG and Failla ML
The Journal of Nutrition, 129(3), 596-601 (1999)

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We offer a variety of small molecule research tools, such as transcription factor modulators, inhibitors of chromatin modifying enzymes, and agonists/antagonists for target identification and validation in gene regulation research; a selection of these research tools is shown below.

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