Purpose: The goal of this study is to identify transcriptome-wide changes that occur in a human prostate cell line with knockdown of MAP3K7(TAK1) and CHD1, in the presence and absence of androgens. We

NIAID Data Ecosystem50

Transcriptome analyses of AR stimulated by 0.1 nM or 10 nM DHT in LNCaP stable cell line overexpressing AR [RNA-Seq]. Transcriptome analyses of AR stimulated by 0.1 nM or 10 nM DHT in LNCaP stable cell line overexpressing AR [RNA-Seq]

前列腺癌分子机制

激素受体信号通路

The molecular drivers for the AR signaling reprogramming in castration-resistant prostate cancer remain to be determined. In this study, we hypothesize that increased AR expression in conjunction with

NIAID Data Ecosystem30

Transcript and protein profiling identify signaling, growth arrest, apoptosis and NFκB-survival signatures following GnRH receptor activation.

癌症分子机制

激素受体信号通路

Gonadotrophin-releasing hormone (GnRH) significantly inhibits proliferation of a proportion of cancer cell lines by activating GnRH receptor-G protein signaling. Therefore, manipulation of GnRH recept

NIAID Data Ecosystem80

Androgen receptor RIP-seq of LNCaP cells treated with androgen hormone. Homo sapiens

激素受体信号通路

lincRNA转录调控

In this work we reported in a high-throughput way (RIP-seq) the RNAs associated with androgen receptor after treatment with androgen hormone. We used a large compilation of lincRNAs to describe the di

NIAID Data Ecosystem50

Genome-wide analysis of androgen receptor (AR) SUMOylation effects on gene expression (HEK293).

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