NF-kB coordinates rapid, BRD4-dependent remodeling of proinflammatory super-enhancers

ChEBI2014-09-29 更新2026-07-21 收录

炎症信号通路

表观遗传调控

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https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-GEOD-54000 数据链接链接失效反馈

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NF-kB coordinates rapid, BRD4-dependent remodeling of proinflammatory super-enhancers

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2014-09-29

Depletion of H3K36me2 recapitulates epigenomic and phenotypic changes induced by the H3.3K36M oncohistone mutation

组蛋白修饰与肿瘤发生

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In this study, our results support a functional divergence between H3K36me2 and H3K36me3 and their non-redundant roles in H3K36M-driven oncogenesis Overall design: 17 ChIP-seq samples, 3 RNA-seq sampl

NIAID Data Ecosystem50

Identification of introduced and stably inherited DNA methylation variants in soybean associated with soybean cyst nematode parasitism [RNA-seq]

大豆抗线虫研究

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Methylome changes mediated by the soybean cyst nematode resistance gene GmSHMT08 Overall design: Examining the changes in the transcriptome of two nearly isogenic lines (TN09-16 and TN09-29) under soy

NIAID Data Ecosystem10

DNMT3A Reads and Connects Histone H3K36me2 to DNA methylation [RNA-seq]

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甲基化反应机制

DNA methylation at the 5-position of cytosine (5mC) is a crucial epigenetic mark in regulating biological processes including gene silencing, gene imprinting, and X chromosome inactivation. It has lon

NIAID Data Ecosystem00

Epigenetic basis for monocyte dysfunction in acute-on-chronic liver failure and alcoholic hepatitis [RNA-seq]

肝病相关单核细胞功能障碍

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BACKGROUND/ AIMS: Severe forms of alcoholic liver disease are associated with increased susceptibility to infections largely due to immune dysfunction. In this study, we analyze the phenotypic, molecu

NIAID Data Ecosystem10

A prion accelerates proliferation at the expense of lifespan

朊病毒与细胞衰老

表观遗传调控

Organisms often commit to one of two strategies: living fast and dying young or living slow and dying old. In fluctuating environments, however, switching between these two strategies could be advanta

Alliance of Genome Resources00

NF-kB coordinates rapid, BRD4-dependent remodeling of proinflammatory super-enhancers

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