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Links from PMC

Items: 9

1.

MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis.[ChIP-Seq]

(Submitter supplied) We performed genome-wide mapping of H3k27ac and H3K4me3 sites in control and MAF-overexpressing MCF7 cells to assess the consequences of estrogen (E2) stimulation and MAF overexpression recruitment to chromatin. To this end, we cultured MCF7 cells in hormone-deprived (HD) medium for 72 h and then E2 or vehicle was added for 1h prior to chromatin immunoprecipitation (ChIP). Samples were generated in triplicate.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL30173
12 Samples
Download data: NARROWPEAK
Series
Accession:
GSE232706
ID:
200232706
2.

MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis.

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL21697 GPL30173
52 Samples
Download data: NARROWPEAK
Series
Accession:
GSE232389
ID:
200232389
3.

MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis [dataset 2]

(Submitter supplied) We mapped chromatin accessibility on control and MAF-overexpressing MCF7 cells to assess the consequences of estrogen (E2, estrogen cepetor (ER) and metastatic MAF expression on the chromatin landscape. To this end, we cultured MCF7 cells in hormone-deprived (HD) medium for 72 h and a specific ER-protac or vehicle was added for 24h for ER degradation. The day after, estrogen (E2) or vehicle was added for 1h prior to DNA purification. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL21697
16 Samples
Download data: XLSX
Series
Accession:
GSE232270
ID:
200232270
4.

MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis [dataset 1]

(Submitter supplied) We performed mRNA profiling of control and MAF-overexpressing MCF7 cells to assess the transcriptional consequences of estrogen receptor (ER) activation upon metastatic MAF expression in the presence or absence or ER (using a protac for ER degradation). To this end, we cultured MCF7 cells in hormone-deprived (HD) medium for 72 h. At this point, we treated the cells with vehice or ER-protac for 24h and then estrogen (E2) or vehicle was added for 6h prior to RNA extraction. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21697
24 Samples
Download data: XLSX
Series
Accession:
GSE232175
ID:
200232175
5.

MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by SNP array; Expression profiling by high throughput sequencing
Platform:
GPL16791
46 Samples
Download data: BED, BEDGRAPH
Series
Accession:
GSE210608
ID:
200210608
6.

MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis [RNA-seq]

(Submitter supplied) We performed mRNA profiling of control and MAF-overexpressing MCF7 cells to assess the transcriptional consequences of estrogen receptor (ER) activation upon metastatic MAF expression. To this end, we cultured MCF7 cells in hormone-deprived (HD) medium for 72 h and then estrogen (E2) or vehicle was added for 6h prior to RNA extraction. Samples were generated in triplicate. We report that MAF supports the expression of genes involved in metastatic functions and that E2 treatment correlates with E2 early and late gene responses and cell cycle regulation. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
16 Samples
Download data: XLSX
Series
Accession:
GSE210607
ID:
200210607
7.

MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis [MAF ChIP-seq]

(Submitter supplied) We performed genome-wide mapping of MAF binding sites in control and MAF-overexpressing MCF7 cells to assess the consequences of estrogen (E2) stimulation on MAF recruitment to chromatin. To this end, we cultured MCF7 cells in hormone-deprived (HD) medium for 72 h and then E2 or vehicle was added for 1h prior to chromatin immunoprecipitation (ChIP). Samples were generated in triplicate. We report that MAF binding is largely independent of E2
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by SNP array
Platform:
GPL16791
6 Samples
Download data: BED, BEDGRAPH
Series
Accession:
GSE210605
ID:
200210605
8.

MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis [ER ChIP-seq]

(Submitter supplied) We performed genome-wide mapping of estrogen receptor (ER) binding sites in control and MAF-overexpressing MCF7 cells to assess the consequences of estrogen (E2) stimulation upon metastasic MAF expression. To this end, we cultured MCF7 cells in hormone-deprived (HD) medium for 72 h and then E2 or vehicle was added for 1h prior to chromatin immunoprecipitation (ChIP). Samples were generated in triplicate. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by SNP array
Platform:
GPL16791
8 Samples
Download data: BED, BEDGRAPH
Series
Accession:
GSE210604
ID:
200210604
9.

MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis [ATAC-seq]

(Submitter supplied) We mapped chromatin accessibility on control and MAF-overexpressing MCF7 cells to assess the consequences of estrogen (E2) and metastatic MAF expression on the chromatin landscape. To this end, we cultured MCF7 cells in hormone-deprived (HD) medium for 72 h and estrogen (E2) or vehicle was added for 1h prior to DNA purification. Samples were generated in quadruplicate. We report changes in chromaitn accessibility depending on both MAF expression and E2 stimulation.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by SNP array
Platform:
GPL16791
16 Samples
Download data: XLSX
Series
Accession:
GSE210603
ID:
200210603
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