<b>Supplemental material</b>

NIAID Data Ecosystem2026-05-02 收录

乳腺癌分子机制

肿瘤代谢调控

数据链接：

https://figshare.com/articles/dataset/_b_Supplemental_material_b_/27957339 数据链接链接失效反馈

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This study identified that USP35 regulates proliferation and glycolysis of breast cancer cells by mediating the ubiquitination level of PFK-1. The USP35/PFK-1 axis offers novel insight for the treatment of breast cancer.

创建时间：

2024-12-04

SMAD3 and SOX4 binding profiling in human breast cell lines. SMAD3 and SOX4 binding profiling in human breast cell lines

转录因子结合分析

乳腺癌分子机制

In order to identify genes co-bound by SOX4 and SMAD3 in the context of breast cancer, different breast cell lines (HMLEs, MDA-MB-231 or HCC-1954) were used. Due to low endogenous expression levels fo

NIAID Data Ecosystem80

The primer sequence.

乳腺癌分子机制

癌症药物靶点

BackgroundBreast cancer continues to be a predominant cause of female mortality globally, characterized by limited therapeutic options and substantial adverse effects. Artesunate (ART), a traditional

Figshare2025-08-04 更新40

TRPS1 modulates chromatin accessibility to regulate estrogen receptor (ER) binding and ER target gene expression in luminal breast cancer cells (Time course PRO-seq). TRPS1 modulates chromatin accessibility to regulate estrogen receptor (ER) binding and ER target gene expression in luminal breast cancer cells (Time course PRO-seq)

乳腺癌分子机制

染色质可及性调控

Breast cancer is the most frequently diagnosed cancer in women. The most common subtype is luminal breast cancer, which is typically driven by the estrogen receptor alpha (ER), a transcription factor

NIAID Data Ecosystem30

The cholesterol metabolite 27-hydroxycholesterol increases the secretion of extracellular vesicles which promote breast cancer progression.

乳腺癌分子机制

代谢与癌症

Supplementary Data for: Title: The cholesterol metabolite 27-hydroxycholesterol increases the secretion of extracellular vesicles which promote breast cancer progression. Authors: Amy E. Baek1,§,*,

NIAID Data Ecosystem50

Dietary ligands diindolylmethane and resveratrol result in diverse ERα signaling not seen after E2 and a subset of diindolylmethane mediated signaling needs concurrent AHR activation.. Dietary ligands diindolylmethane and resveratrol result in diverse ERα signaling not seen after E2 and a subset of diindolylmethane mediated signaling needs concurrent AHR activation.

乳腺癌分子机制

受体信号通路

Inhibitory crosstalk between estrogen receptor alpha (ER alpha ) and aryl hydrocarbon receptor (AHR) regulates 17-estradiol (E2)-dependent breast cancer cell signaling. ER alpha and AHR are transcript

NIAID Data Ecosystem40

<b>Supplemental material</b>

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