ChIP seq for H4K5ac, JunD , and MED1 in Parental and Paclitaxel resistant L3.6pl cell line

ChEBI2023-03-21 更新2026-07-12 收录

表观遗传学分析

化疗耐药机制

数据链接：

https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-MTAB-12707 数据链接链接失效反馈

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ChIP seq for H4K5ac, JunD , and MED1 in Parental and Paclitaxel resistant L3.6pl cell line

创建时间：

2023-03-21

Mint-ChIP-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR656EAG)

表观遗传学分析

T细胞免疫研究

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表观遗传学分析

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化疗耐药机制

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化疗耐药机制

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Unveiling alterations of epigenetic modifications and chromatin architecture leading to lipid metabolic reprogramming during the evolutionary trastuzumab adaptation of HER2-positive breast cancer [Cut & Tag]. Unveiling alterations of epigenetic modifications and chromatin architecture leading to lipid metabolic reprogramming during the evolutionary trastuzumab adaptation of HER2-positive breast cancer [Cut & Tag]

化疗耐药机制

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Secondary trastuzumab resistance represents an evolutionary adaptation of HER2-positive breast cancer during anti-HER2 treatment. Most current studies have uncovered the alternations of HER2 and assoc

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ChIP seq for H4K5ac, JunD , and MED1 in Parental and Paclitaxel resistant L3.6pl cell line

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