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Series GSE30931 Query DataSets for GSE30931
Status Public on Nov 22, 2011
Title Proteasome inhibition blocks estrogen-dependent gene transcription by decreasing histone H2B monoubiquitination in human breast cancer cells
Organism Homo sapiens
Experiment type Expression profiling by array
Summary The estrogen receptor-alpha (ERα) determines breast cancer cell phenotype and is a prognostic indicator. A better understanding of the mechanisms controlling ERα function may uncover improved strategies for the treatment of breast cancer. Proteasome inhibition was previously reported to regulate estrogen-induced transcription but the mechanisms by which it influences ERα function remain controversial. In this study we investigated the transcriptome-wide effects of the proteasome inhibitor Velcade on estrogen-regulated transcription in MCF7 human breast cancer cells and demonstrate a specific global decrease in estrogen-induced transcription.
 
Overall design This set contains 12 microarray samples. 3 controls, 3 estrogen stimulated, 3 Bortezomib stimulated, 3 Bortezomib + estrogen stimulated
 
Contributor(s) Prenzel T, Begus-Nahrmann Y, Kramer F, Hennion M, Hsu C, Gorsler T, Hintermayr C, Eick D, Kremmer E, Simons M, Beissbarth T, Johnsen SA
Citation(s) 21862633
Submission date Jul 25, 2011
Last update date Aug 13, 2018
Contact name Frank Kramer
E-mail(s) [email protected]
Organization name University Medical Center Göttingen
Department Department of Medical Statistics
Street address Humboldtallee 32
City Goettingen
ZIP/Postal code 37073
Country Germany
 
Platforms (1)
GPL10558 Illumina HumanHT-12 V4.0 expression beadchip
Samples (12)
GSM766676 Cont G1
GSM766677 Cont G2
GSM766678 Cont G3
Relations
BioProject PRJNA146281

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE30931_RAW.tar 26.2 Mb (http)(custom) TAR
GSE30931_non-normalized.txt.gz 2.0 Mb (ftp)(http) TXT
Processed data included within Sample table

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