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The miR-96 and RARG signaling axis governs androgen signaling and prostate cancer progression V
PubMed Full text in PMC Similar studies Analyze with GEO2RSRA Run Selector
The miR-96 and RARG signaling axis governs androgen signaling and prostate cancer progression
PubMed Full text in PMC Similar studies Analyze with GEO2R
The miR-96 and RARG signaling axis governs androgen signaling and prostate cancer progression VI
PubMed Full text in PMC Similar studies SRA Run Selector
The miR-96 and RARG signaling axis governs androgen signaling and prostate cancer progression IV
The miR-96 and RARG signaling axis governs androgen signaling and prostate cancer progression III
The miR-96 and RARG signaling axis governs androgen signaling and prostate cancer progression II
The miR-96 and RARG signaling axis governs androgen signaling and prostate cancer progression I
SOCS2 expression correlates with tumor malignancy, exerts growth promoting effects and is enhanced by androgens in prostate cancer
Identification of hsa-miR-135a target genes in LNCaP and HeLa cell lines
PubMed Similar studies Analyze with GEO2R
Identification of hsa-miR-135a target genes in the HeLa cell line
Identification of hsa-miR-135a target genes in the prostate cancer cell line LNCaP
A Novel Androgen Receptor Splice Variant Is Upregulated during Prostate Cancer Progression
LincRNA PVT1 associates with EZH2 and with the androgen receptor in LNCaP prostate cancer cells and inhibits the expression of genes involved with cell death, cell differentiation and cell adhesion
Darolutamide antagonizes androgen signaling by blocking enhancer and super-enhancer activation
PubMed Full text in PMC Similar studies
Darolutamide antagonizes androgen signaling by blocking enhancer and super-enhancer activation [RNA-seq]
Darolutamide antagonizes androgen signaling by blocking enhancer and super-enhancer activation [ChIP-seq]
Hormone-Independence of Prostate Cancer Cells is Supported by the Androgen Receptor without Binding to Classical Response Elements
Late passage LNCaP prostate tumor cells treated with androgen receptor shRNA or androgen R1881
PubMed Full text in PMC Similar studies GEO Profiles Analyze DataSet
Overexpression of c-Myc antagonises transcriptional output of the androgen receptor in prostate cancer
Overexpression of c-Myc antagonises transcriptional output of the androgen receptor in prostate cancer [ChIP-Seq]
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