Investigating the effect of CDK inhibition in EML4-ALK cells by ChIP-seq for RNA polymerase II.

ChEBI2020-05-13 更新2026-07-12 收录

靶向治疗机制

转录调控与表观遗传学

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Investigating the effect of CDK inhibition in EML4-ALK cells by ChIP-seq for RNA polymerase II.

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2020-05-13

Cancer Type-Specific SPOP Mutants Alter BET Protein Levels and Inhibitor Responses

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泛素化调控与药物响应

It is generally assumed that recurrent mutations within a given cancer driver gene elicit similar drug responses. Recently, cancer genome studies have delineated recurrent but divergent missense mutat

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Impact of ALK inhibition or phospho-deficient mutation of CDK9 on gene expression in ovarian cancer cells

卵巢癌基因表达

靶向治疗机制

The goal of this study is to determine the impact of ALK inhibition or phospho-deficient mutation of CDK9 on gene expresion profiles in ovarian cancer cells We performed bulk RNA sequencing on three c

NIAID Data Ecosystem50

Molecular Chaperone RUVBL2 Activates Oncogenes by Modulation of Transcriptional Condensates [Mnase-seq]

转录调控

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Transcription regulators and apparatuses compartmentalize into transcriptional condensates in part through molecular interactions among intrinsically disordered regions. To better understand how these

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Amplicon-Dependent CCNE1 Expression Is Critical for Clonogenic Survival after Cisplatin Treatment and Is Correlated with 20q11 Gain in Ovarian Cancer

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Genomic amplification of 19q12 occurs in several cancer types including ovarian cancer where it is associated with primary treatment failure. We systematically attenuated expression of genes within th

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Global chromatin occupancy and epigenetic signature analysis reveal new insights into the function of GATA1 N-terminus in erythropoiesis

红细胞生成分子机制

转录调控与表观遗传学

Mutations in GATA1, which lead to expression of the GATA1s isoform that lacks the GATA1 N-terminus, are seen in patients with Diamond-Blackfan Anemia (DBA). In our efforts to better understand the con

NIAID Data Ecosystem50

Investigating the effect of CDK inhibition in EML4-ALK cells by ChIP-seq for RNA polymerase II.

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