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Updated: Mar 22, 2026

Dissection of Enhancer Function Using Multiplex CRISPR-based Enhancer Interference in Cell Lines
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RACK7-ヒストンデメチラーゼ複合体によるエンハンサー過剰活性化の抑制

Hongjie Shen1, Wenqi Xu1, Rui Guo2

  • 1Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, and Key Laboratory of Epigenetics, Department of Cellular and Genetic Medicine, School of Basic Medical Sciences and Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China; Key Laboratory of Birth Defect, Children's Hospital of Fudan University, Shanghai 201102, China.

Cell
|April 9, 2016
PubMed
まとめ

RACK7/KDM5C複合体は増強ブレーキとして作用し,遺伝子発現を制御します. その喪失は増強剤の過剰活性化につながり,腫瘍遺伝子を抑制することによって癌の発生を促進します.

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The histone proteins in the nucleosomes are post-translationally modified (PTM) to increase or decrease access to DNA. The commonly observed PTMs are methylation, acetylation, phosphorylation, and ubiquitination of lysine amino acids in the histone H3 tail region. These histone modifications have specific meaning for the cell. Hence, they are called "histone code". The protein complex involved in histone modification is termed as "reader-writer" complex.
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