NMT inhibition in the context of MYC levels
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE154336 | GEO | 2022/06/30
REPOSITORIES: GEO
Similar Datasets
Project description:NMT inhibition in the context of MYC levels
| PRJNA645908 | ENA
Project description:P493-6 cells are immortalized human peripheral B cells that carry a conditional, tetracycline-regulated myc gene. We present ChIP-seq analysis of key transcritional regulators in P493-6 cells expressing various levels of c-Myc: 0hr (low c-Myc levels), 1hr (intermediate c-Myc levels), 24hr (very high c-Myc levels) and No Tet (steady-state c-Myc levels). Brd4, c-Myc, Max, Med1, RNAPII, and the chromatin modification H3K27Ac were profiled in P493-6 cells
2012-11-14 | E-GEOD-42262 | biostudies-arrayexpress
Project description:P493-6 cells are immortalized human peripheral B cells that carry a conditional, tetracycline-regulated myc gene. We present ChIP-seq analysis of key transcritional regulators in P493-6 cells expressing various levels of c-Myc: 0hr (low c-Myc levels), 1hr (intermediate c-Myc levels), 24hr (very high c-Myc levels) and No Tet (steady-state c-Myc levels).
2012-11-14 | GSE42262 | GEO
Project description:Myc is a well known transcription factor with important roles in cell cycle, apoptosis and cellular transformation. Long non-coding (lnc)RNAs have recently emerged as a important class of regulatory RNAs. Here, we show that lncRNAs are an extensive component of the Myc-regulated transcriptional program. Using the P493-6 inducible Myc model we demonstrate that both Myc-induced mRNAs and lncRNAs were significant enriched for Myc binding sites. In contrast to Myc-repressed mRNAs, Myc-repressed lncRNAs were significantly enriched for Myc binding sites. Subcellular localization analysis revealed that Myc-repressed lncRNAs and mRNAs are enriched in the nucleus while Myc-induced lncRNAs and mRNAs are enriched both in the cytoplasm and nucleus. Parallel analysis of differentially expressed lncRNAs and mRNAs identified 105 lncRNA-mRNA pairs that were in close vicinity, indicative for regulation in cis. To support the potential relevance of the Myc-regulated lncRNAs in cellular transformation, we analyzed their expression in primary Myc-high and Myc-low B-cell lymphomas. In total, 54% of the lncRNAs differentially expressed between the lymphoma subsets were identified as Myc-regulated in P493-6 cells. This study is the first to show that lncRNAs are an important factor within the Myc-regulated transcriptional program and indicates a marked difference between Myc-repressed lncRNAs and mRNAs. P493-6: 72h Tet treated (low c-myc levels), t=4h (intermediate c-myc levels), t=24h (high c-myc levels), untreated (steady state c-myc levels) Expression of all known mRNAs and >10 000 lncRNAs was assessed in P493-6 B cells with different c-myc levels
2015-02-01 | E-GEOD-59477 | biostudies-arrayexpress
Project description:Myc is a well known transcription factor with important roles in cell cycle, apoptosis and cellular transformation. Long non-coding (lnc)RNAs have recently emerged as a important class of regulatory RNAs. Here, we show that lncRNAs are an extensive component of the Myc-regulated transcriptional program. Using the P493-6 inducible Myc model we demonstrate that both Myc-induced mRNAs and lncRNAs were significant enriched for Myc binding sites. In contrast to Myc-repressed mRNAs, Myc-repressed lncRNAs were significantly enriched for Myc binding sites. Subcellular localization analysis revealed that Myc-repressed lncRNAs and mRNAs are enriched in the nucleus while Myc-induced lncRNAs and mRNAs are enriched both in the cytoplasm and nucleus. Parallel analysis of differentially expressed lncRNAs and mRNAs identified 105 lncRNA-mRNA pairs that were in close vicinity, indicative for regulation in cis. To support the potential relevance of the Myc-regulated lncRNAs in cellular transformation, we analyzed their expression in primary Myc-high and Myc-low B-cell lymphomas. In total, 54% of the lncRNAs differentially expressed between the lymphoma subsets were identified as Myc-regulated in P493-6 cells. This study is the first to show that lncRNAs are an important factor within the Myc-regulated transcriptional program and indicates a marked difference between Myc-repressed lncRNAs and mRNAs. P493-6: 72h Tet treated (low c-myc levels), t=4h (intermediate c-myc levels), t=24h (high c-myc levels), untreated (steady state c-myc levels)
2015-02-01 | GSE59477 | GEO
Project description:Ectopic Myc Expression in P493-6 B-cells at three levels: High Myc, Low Myc and No Myc
2010-02-25 | GSE19703 | GEO
Project description:Ectopic Myc Expression in P493-6 B-cells at three levels: High Myc, Low Myc and No Myc High Myc, Low Myc and No Myc expressions
2010-03-09 | E-GEOD-19703 | biostudies-arrayexpress
Project description:p493 RNA-seq in the MYC on and MYC off conditions
2018-09-21 | GSE120246 | GEO
Project description:Trimethylated H3K4 (H3K4me3), which is often found surrounding the transcriptional start site of active genes, is strongly enriched in the promoter regions of Myc-targeted genes. Succinate, which inhibits JmjC domain-containing histone demethylases (JHDMs), can induce H3K4me3 level of the promoter regions. It's interesting to ask whether Myc can mediate H3K4me3 by inhibiting SDH activity and inducing cellular succinate level. Here, We used ChIP-seq to study Myc modulates H3K4me3 by altering succinate levels, dimethyl succinate (DMS), a membrane-permeable succinate analog, was introduced to treat P493-6 cells with high or depleted Myc expression. And we performed RNA-seq assays in Myc expressed or depleted P493-6 cells with or without DMS treatment. Besides, we also performed RNA-seq assays in Myc expressed or depleted P493-6 cells with or without 3-nitropropionic acid (3-NPA, SDH enzyme inhibitor) treatment.
2020-03-18 | GSE124255 | GEO
Project description:The c-myc proto-oncogene product, Myc, is a transcription factor that binds thousands of genomic loci. Recent work suggested that rather than up- and down-regulating selected groups of genes, Myc targets all active promoters and enhancers in the genome (a phenomenon termed "invasion") and acts as a general amplifier of transcription. However, the available data did not readily discriminate between direct and indirect effects of Myc on RNA biogenesis. We addressed this issue with genome-wide chromatin immunoprecipitation and RNA expression profiles during B-cell lymphomagenesis in mice, in cultured B-cells and fibroblasts. Consistent with long-standing observations, we detected general increases in total RNA or mRNA copies per cell (hereby termed "amplification") when comparing actively proliferating cells with control quiescent cells: this was true whether cells were stimulated by mitogens (requiring endogenous Myc for a proliferative response) or by deregulated, oncogenic Myc activity. RNA amplification and promoter/enhancer invasion by Myc were separable phenomena that could occur without one another. Moreover, whether or not associated with RNA amplification, Myc drove the differential expression of distinct subsets of target genes. Hence, while having the potential to interact with all active/poised regulatory elements in the genome, Myc does not directly act as a global transcriptional amplifier. Instead, our results imply that Myc activates and represses transcription of discrete gene sets, leading to changes in cellular state that can in turn feed back on global RNA production and turnover. Mapping c-Myc, RNAPII and H3K4me3, H3K4me1 and H3K27ac in four different models of Myc regulation Note: GEO Sample GSM894093 was used as input sample to generate processed data files P493.Myc.NoMyc.bed, P493.Myc.LowMyc.bed, P493.Myc.HighMyc.bed, P493.Myc.t1h.bed, P493.Myc.t24h.bed, P493.Pol2.NoMyc.bed, P493.Pol2.t24h.bed
2014-07-07 | E-GEOD-51004 | biostudies-arrayexpress