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SEC inhibitor KL-1 Sale

(Synonyms: KL-1) 目录号 : GC38063

SEC inhibitor KL-1 (KL-1) is a potent and selective inhibitor of super elongation complex (SEC) that disrupts the interaction between the SEC scaffolding protein AFF4 and P-TEFb, resulting in impaired release of Pol II from promoter-proximal pause sites and a reduced average rate of processive transcription elongation. KL-1 exhibits an dose-dependent inhibitory effect on AFF4-CCNT1 interaction with Ki of 3.48 μM.

SEC inhibitor KL-1 Chemical Structure

Cas No.:900308-84-1

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1mg
¥510.00
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5mg
¥1,530.00
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10mg
¥2,430.00
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25mg
¥3,643.00
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50mg
¥6,750.00
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100mg
¥8,820.00
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Sample solution is provided at 25 µL, 10mM.

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产品描述

SEC inhibitor KL-1 (KL-1) is a potent and selective inhibitor of super elongation complex (SEC) that disrupts the interaction between the SEC scaffolding protein AFF4 and P-TEFb, resulting in impaired release of Pol II from promoter-proximal pause sites and a reduced average rate of processive transcription elongation. KL-1 exhibits an dose-dependent inhibitory effect on AFF4-CCNT1 interaction with Ki of 3.48 μM.

[1] Kaiwei Liang, et al. Cell. 2018 Oct 18;175(3):766-779.e17.

Chemical Properties

Cas No. 900308-84-1 SDF
别名 KL-1
Canonical SMILES O=C(NC1=CC(Cl)=CC=C1C)/C(O)=C/C(C2=CC=CC(OC)=C2)=O
分子式 C18H16ClNO4 分子量 345.78
溶解度 DMSO: 41.67 mg/mL (120.51 mM) 储存条件 Store at -20°C
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1 mg 5 mg 10 mg
1 mM 2.892 mL 14.4601 mL 28.9201 mL
5 mM 0.5784 mL 2.892 mL 5.784 mL
10 mM 0.2892 mL 1.446 mL 2.892 mL
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Research Update

Acute perturbation strategies in interrogating RNA polymerase II elongation factor function in gene expression

Genes Dev 2021 Feb 1;35(3-4):273-285.PMID:33446572DOI:PMC7849361

The regulation of gene expression catalyzed by RNA polymerase II (Pol II) requires a host of accessory factors to ensure cell growth, differentiation, and survival under environmental stress. Here, using the auxin-inducible degradation (AID) system to study transcriptional activities of the bromodomain and extraterminal domain (BET) and super elongation complex (SEC) families, we found that the CDK9-containing BRD4 complex is required for the release of Pol II from promoter-proximal pausing for most genes, while the CDK9-containing SEC is required for activated transcription in the heat shock response. By using both the proteolysis targeting chimera (PROTAC) dBET6 and the AID system, we found that dBET6 treatment results in two major effects: increased pausing due to BRD4 loss, and reduced enhancer activity attributable to BRD2 loss. In the heat shock response, while auxin-mediated depletion of the AFF4 subunit of the SEC has a more severe defect than AFF1 depletion, simultaneous depletion of AFF1 and AFF4 leads to a stronger attenuation of the heat shock response, similar to treatment with the SEC inhibitor KL-1, suggesting a possible redundancy among SEC family members. This study highlights the usefulness of orthogonal acute depletion/inhibition strategies to identify distinct and redundant biological functions among Pol II elongation factor paralogs.