Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A transcription factor addiction imposed by an oncogene promoter sequence [ChIP-seq]

ABSTRACT: Genome-wide binding/occupancy profiling by high throughput sequencing

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE115236 | GEO | 2018/10/26

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

A transcription factor addiction imposed by an oncogene promoter sequence [RNA-seq]

Project description:Transcriptome analysis by high throughput sequencing

2018-10-26 | GSE115237 | GEO

A transcription factor addiction imposed by an oncogene promoter sequence

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-10-26 | GSE115238 | GEO

A Transcription Factor Addiction in Leukemia Imposed by the MLL Promoter Sequence.

Project description:The Mixed Lineage Leukemia gene (MLL) is altered in leukemia by chromosomal translocations to produce oncoproteins composed of the MLL N-terminus fused to the C-terminus of a partner protein. Here, we used domain-focused CRISPR screening to identify ZFP64 as an essential transcription factor in MLL-rearranged leukemia. We show that the critical function of ZFP64 in leukemia is to maintain MLL expression via binding to the MLL promoter, which is the most enriched location of ZFP64 occupancy in the human genome. The specificity of ZFP64 for MLL is accounted for by an exceptional density of ZFP64 motifs embedded within the MLL promoter. These findings demonstrate how a sequence anomaly of an oncogene promoter can impose a transcriptional addiction in cancer.

| S-EPMC6554023 | biostudies-literature

A transcription factor addiction imposed by an oncogene promoter sequence

Project description:A transcription factor addiction imposed by an oncogene promoter sequence

| PRJNA474222 | ENA

A transcription factor addiction imposed by an oncogene promoter sequence [ChIP-seq]

Project description:A transcription factor addiction imposed by an oncogene promoter sequence [ChIP-seq]

| PRJNA474225 | ENA

A transcription factor addiction imposed by an oncogene promoter sequence [RNA-seq]

Project description:A transcription factor addiction imposed by an oncogene promoter sequence [RNA-seq]

| PRJNA474224 | ENA

Antiproliferative small-molecule inhibitors of transcription factor LSF reveal oncogene addiction to LSF in hepatocellular carcinoma.

Project description:Hepatocellular carcinoma (HCC) is the fifth most common cancer worldwide. Despite the prevalence of HCC, there is no effective, systemic treatment. The transcription factor LSF is a promising protein target for chemotherapy; it is highly expressed in HCC patient samples and cell lines, and promotes oncogenesis in rodent xenograft models of HCC. Here, we identify small molecules that effectively inhibit LSF cellular activity. The lead compound, factor quinolinone inhibitor 1 (FQI1), inhibits LSF DNA-binding activity both in vitro, as determined by electrophoretic mobility shift assays, and in cells, as determined by ChIP. Consistent with such inhibition, FQI1 eliminates transcriptional stimulation of LSF-dependent reporter constructs. FQI1 also exhibits antiproliferative activity in multiple cell lines. In LSF-overexpressing cells, including HCC cells, cell death is rapidly induced; however, primary or immortalized hepatocytes are unaffected by treatment with FQI1. The highly concordant structure-activity relationship of a panel of 23 quinolinones strongly suggests that the growth inhibitory activity is due to a single biological target or family. Coupled with the striking agreement between the concentrations required for antiproliferative activity (GI(50)s) and for inhibition of LSF transactivation (IC(50)s), we conclude that LSF is the specific biological target of FQIs. Based on these in vitro results, we tested the efficacy of FQI1 in inhibiting HCC tumor growth in a mouse xenograft model. As a single agent, tumor growth was dramatically inhibited with no observable general tissue cytotoxicity. These findings support the further development of LSF inhibitors for cancer chemotherapy.

| S-EPMC3311344 | biostudies-literature

RUNX1 transcription factor genome-wide occupancy in EML cells

Project description:We report the application of sequencing technology for high-throughput profiling of RUNX1 transcription factor occupancy in mouse EML cells. RUNX1 antibody was use for chromatin immunoprecipitation followed by high-throughput sequencing to reveal RUNX1 genome occupancy in hematopoietic stem/progenitor cells.

2014-10-24 | GSE62596 | GEO

Role of promoter DNA sequence variations on the binding of EGR1 transcription factor.

Project description:In response to a wide variety of stimuli such as growth factors and hormones, EGR1 transcription factor is rapidly induced and immediately exerts downstream effects central to the maintenance of cellular homeostasis. Herein, our biophysical analysis reveals that DNA sequence variations within the target gene promoters tightly modulate the energetics of binding of EGR1 and that nucleotide substitutions at certain positions are much more detrimental to EGR1-DNA interaction than others. Importantly, the reduction in binding affinity poorly correlates with the loss of enthalpy and gain of entropy-a trend indicative of a complex interplay between underlying thermodynamic factors due to the differential role of water solvent upon nucleotide substitution. We also provide a rationale for the physical basis of the effect of nucleotide substitutions on the EGR1-DNA interaction at atomic level. Taken together, our study bears important implications on understanding the molecular determinants of a key protein-DNA interaction at the cross-roads of human health and disease.

| S-EPMC4006273 | biostudies-literature

RUNX1 transcription factor genome-wide occupancy in EML cells

2014-10-24 | E-GEOD-62596 | biostudies-arrayexpress