Dopamine Signaling leads to loss of Polycomb Repression and Aberrant Gene

ChEBI2014-10-01 更新2026-07-21 收录

神经肽信号传导

表观遗传调控

数据链接：

https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-GEOD-60703 数据链接链接失效反馈

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Dopamine Signaling leads to loss of Polycomb Repression and Aberrant Gene

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2014-10-01

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

表观遗传调控

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

Transcriptional Dynamics of Skeletal Muscle in Obesity (PRJCA023478)

肥胖相关转录组学

表观遗传调控

Skeletal muscle is a metabolically active organ, but it remains largely unexplored in obesity. Here, we used diet-induced mice as obesity model to investigate the effect of obesity on muscle transcrip

NIAID Data Ecosystem00

ARID1B regulates BCL11B-mediated non-canonical Activin signaling to maintain mesenchymal stem cell homeostasis in the mouse incisor [scRNA-seq]

干细胞稳态

表观遗传调控

ARID1B is a epigenetic regulator. We used the scRNA sequencing to analysis the role of ARID1B in regulating mouse incisor tissue homeostasis. Single-cell transcriptomes were obtained from the digested

NIAID Data Ecosystem00

mRNA profiling of Pontin WT and RA under glucose starvation

表观遗传调控

葡萄糖饥饿应激

To determine which genes are affected by methylated Pontin, we performed RNA-sequencing (RNA-seq) in Pontin WT and RA MEFs after glucose starvation. Overall design: mRNA expression profiles of Pontin

NIAID Data Ecosystem10

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

表观遗传调控

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

Dopamine Signaling leads to loss of Polycomb Repression and Aberrant Gene

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