{"owner": "ArrayExpress Uploader", "ownerprofile_id": "arrayexpress_sid", "id": 6543, "factors": [{"GSM765953": {"GENOTYPE/VARIATION": "infected with retroviruses expressing H-RasV12"}}, {"GSM765954": {"GENOTYPE/VARIATION": "infected with retroviruses expressing H-RasV13"}}, {"GSM765955": {"GENOTYPE/VARIATION": "infected with retroviruses expressing H-RasV14"}}, {"GSM765956": {"GENOTYPE/VARIATION": "infected with retroviruses expressing H-RasV12 and C/EBP\u03b2"}}, {"GSM765956": {"GENOTYPE/VARIATION": "infected with retroviruses expressing H-RasV12 and C/EBP\u03b2"}}, {"GSM765956": {"GENOTYPE/VARIATION": "infected with retroviruses expressing H-RasV12 and C/EBP\u03b2"}}, {"GSM765959": {"GENOTYPE/VARIATION": "infected with retroviruses expressing H-RasV12 and C/EBP\u03b2-UTR"}}, {"GSM765959": {"GENOTYPE/VARIATION": "infected with retroviruses expressing H-RasV12 and C/EBP\u03b2-UTR"}}, {"GSM765959": {"GENOTYPE/VARIATION": "infected with retroviruses expressing H-RasV12 and C/EBP\u03b2-UTR"}}], "pop_total": 0, "platform": 6, "summary_wrapped": "C/EBPb is an auto-repressed protein that becomes posttranslationally activated by Ras-MEK-ERK signalling. C/EBPb is required for...", "geo_gse_id": "E-GEOD-30834", "owner_profile": "/profile/8773/arrayexpressuploader", "factor_count": 1, "sample_count": 9, "tags": ["protein"], "lastmodified": "Dec.12, 2014", "is_default": false, "geo_gds_id": "", "slug": "influence-of-cebp-3utr-on-rasv12-induced-gene-expr", "geo_id_plat": "E-GEOD-30834_A-AFFY-45", "name": "Influence of C/EBP\u03b2 3'UTR on RasV12 induced gene expression", "created": "Nov.11, 2014", "summary": "C/EBPb is an auto-repressed protein that becomes posttranslationally activated by Ras-MEK-ERK signalling. C/EBPb is required for oncogene-induced senescence (OIS) of primary fibroblasts, but also displays pro-oncogenic functions in many tumour cells. Here, we show that C/EBPb activation by H-RasV12 is suppressed in immortalized/transformed cells, but not in primary cells, by its 30 untranslated region (30UTR). 30UTR sequences inhibited Ras-induced cytostatic activity of C/EBPb, DNA binding, transactivation, phosphorylation, and homodimerization, without significantly affecting protein expression. The 30UTR suppressed induction of senescence-associated C/EBPb target genes, while promoting expression of genes linked to cancers and TGFb signalling. An AU-rich element (ARE) and its cognate RNA-binding protein, HuR, were required for 30UTR inhibition. These components also excluded the Cebpb mRNA from a perinuclear cytoplasmic region that contains activated ERK1/2, indicating that the site of C/EBPb translation controls de-repression by Ras signalling. Notably, 30UTR inhibition and Cebpb mRNA compartmentalization were absent in primary fibroblasts, allowing Ras-induced C/EBPb activation and OIS to proceed. Our findings reveal a novel mechanism whereby non-coding mRNA sequences selectively regulate C/EBPb activity and suppress its anti-oncogenic functions. NIH-3T3 cells were retrovirally infected and selected with appropriate antiobiotics.  Equal number of cells were plated and collected 48-72 hours later.", "source": "http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-30834", "species": "mouse", "sample_source": "http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-30834/samples/"}