Targeting EZH2 methyltransferase activity in ARID1A mutated cells as a synthetic lethal therapeutic strategy

ChEBI2015-01-20 更新2026-07-21 收录

合成致死治疗

表观遗传靶向治疗

数据链接：

https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-GEOD-54979 数据链接链接失效反馈

官方服务：

资源简介：

Targeting EZH2 methyltransferase activity in ARID1A mutated cells as a synthetic lethal therapeutic strategy

创建时间：

2015-01-20

Inhibitors of Rho kinases (ROCK) induce multiple mitotic defects and synthetic lethality in BRCA2-deficient cells

细胞有丝分裂缺陷

合成致死治疗

 The trapping of Poly-ADP-ribose polymerase (PARP) on DNA caused by PARP inhibitors (PARPi) triggers acute DNA replication stress and synthetic lethality (SL) in BRCA2-deficient cells. Hence, DNA

DataONE2026-04-13 更新50

Structure-Guided Design of IACS-9571, a Selective High-Affinity Dual TRIM24-BRPF1 Bromodomain Inhibitor

溴结构域抑制剂

表观遗传靶向治疗

The bromodomain containing proteins TRIM24 (tripartite motif containing protein 24) and BRPF1 (bromodomain and PHD finger containing protein 1) are involved in the epigenetic regulation of gene expres

NIAID Data Ecosystem50

Suppression of the CIC-DUX4 oncogene through p300/CBP inhibition. Suppression of the CIC-DUX4 oncogene through p300/CBP inhibition

表观遗传靶向治疗

儿童肉瘤药物研发

A recently identified pediatric subtype of undifferentiated round cell sarcoma that is driven by fusion between the cell cycle regulator and transcriptional repressor, capicula (CIC) and the transcrip

NIAID Data Ecosystem30

MTA-Cooperative PRMT5 Inhibitors: Mechanism Switching Through Structure-Based Design

表观遗传学药物设计

合成致死治疗

Deletion of the MTAP gene leads to accumulation of the substrate of the MTAP protein, methylthioadenosine (MTA). MTA binds PRMT5 competitively with S-adenosyl-l-methionine (SAM), and selective inhibit

Figshare2025-02-07 更新50

Neuroendocrine lineage commitment of small cell lung cancers can be leveraged into p53-independent non-cytotoxic therapy [RNA-seq]. Neuroendocrine lineage commitment of small cell lung cancers can be leveraged into p53-independent non-cytotoxic therapy [RNA-seq]

小细胞肺癌分子机制

表观遗传靶向治疗

Small cell lung cancers (SCLC) rapidly resist cytotoxic chemotherapy and immune-checkpoint inhibitor (ICI) treatments. New, non-cross-resistant therapies are thus needed. SCLC cells are committed into

NIAID Data Ecosystem30

Targeting EZH2 methyltransferase activity in ARID1A mutated cells as a synthetic lethal therapeutic strategy

资源简介：

相关数据集