EZH2 Overexpression in Breast Cancer is due to MicroRNA-Dependent Suppression of ZBTB4

ChEBI2015-03-02 更新2026-07-21 收录

乳腺癌分子机制

表观遗传调控

数据链接：

https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-GEOD-48979 数据链接链接失效反馈

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EZH2 Overexpression in Breast Cancer is due to MicroRNA-Dependent Suppression of ZBTB4

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2015-03-02

Multimodal learning of noncoding variant effects using genome sequence and chromatin structure

变异功能预测

表观遗传调控

ncVarPred-1D3D: pretrained models of Sei (PMID: 35817977) + our 3D structure embedding models are shared. The models are trained and validated using DeepSEA (PMID: 26301843) selected 200 bp regions (w

Zenodo2023-08-08 更新00

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

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Multiple Nucleosome Positioning Sites Regulate the CTCF-Mediated Insulator Function of the H19 Imprinting Control Region†

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染色质绝缘子功能

The 5′ region of the H19 gene harbors a methylation-sensitive chromatin insulator within an imprinting control region (ICR). Insertional mutagenesis in combination with episomal assays identified nucl

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ChIP Seq of influenza specific primary, memory and secondary CD4+ T cells [InVitro]

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CD4+T细胞记忆

Immune responses to infection involve a careful balance: too weak a response allows pathogen replication; too strong risks immunopathology. The immunoregulatory cytokine IL-10 is a key factor in this

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ZDHHC15 mediates Hippo/YAP pathway palmitoylation and regulates tumor progression [TOV-112D]. ZDHHC15 mediates Hippo/YAP pathway palmitoylation and regulates tumor progression [TOV-112D]

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YAP信号通路

The Post-translational modification of Hippo/YAP pathway members plays an important role in regulating the activation of Hippo/YAP pathway and its effects in tumors. S-Palmitoylation, also known as S-

NIAID Data Ecosystem00

EZH2 Overexpression in Breast Cancer is due to MicroRNA-Dependent Suppression of ZBTB4

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