Similar Datasets
Project description:STAU2 knockdown in human K562 cells
2020-04-21 | GSE135012 | GEO
Project description:Stau2 knockdown in human bcCML cells (K562)"
| PRJNA557137 | ENA
Project description:Effect of Stau2 knockdown on H3K4 methylation in human bcCML cells (K562)
| PRJNA596503 | ENA
Project description:FOXA1 is a pioneer factor that is important in hormone dependent cancer cells to stabilise nuclear receptors, such as estrogen receptor (ER) to chromatin. FOXA1 binds to enhancers regions that are enriched in H3K4mono- and dimethylation (H3K4me1, H3K4me2) histone marks and evidence suggests that these marks are requisite events for FOXA1 to associate with enhancers to initate subsequent gene expression events. However, exogenous expression of FOXA1 has been shown to induce H3K4me1 and H3K4me2 signal at enhancer elements and the order of events and the functional importance of these events is not clear. We performed a FOXA1 Rapid Immunoprecipitation Mass Spectrometry of Endogenous Proteins (RIME) screen in ERα-positive MCF-7 breast cancer cells in order to identify FOXA1 interacting partners and we found histone-lysine N-methyltransferase (MLL3) as the top FOXA1 interacting protein. MLL3 is typically thought to induce H3K4me3 at promoter regions, but recent findings suggest it may contribute to H3K4me1 deposition, in line with our observation that MLL3 associates with an enhancer specific protein. We performed MLL3 ChIP-seq in breast cancer cells and unexpectedly found that MLL3 binds mostly at non-promoter regions enhancers, in contrast to the prevailing hypothesis. MLL3 was shown to occupy regions marked by FOXA1 occupancy and as expected, H3K4me1 and H3K4me2. MLL3 binding was dependent on FOXA1, indicating that FOXA1 recruits MLL3 to chromatin. Motif analysis and subsequent genomic mapping revealed a role for Grainy head like protein-2 (GRHL2) which was shown to co-occupy regions of the chromatin with MLL3. Regions occupied by all three factors, namely FOXA1, MLL3 and GRHL2, were most enriched in H3K4me1. MLL3 silencing decreased H3K4me1 at enhancer elements, but had no appreciable impact on H3K4me3 at enhancer elements. We identify a complex relationship between FOXA1, MLL3 and H3K4me1 at enhancers in breast cancer and propose a mechanism whereby the pioneer factor FOXA1 can interact with a chromatin modifier MLL3, recruiting it to chromatin to facilitate the deposition of H3K4me1 histone marks, subsequently demarcating active enhancer elements.
2016-12-12 | PXD005253 | Pride
Project description:The double-stranded RNA binding protein Staufen2 (Stau2) is asymmetrically localized and segregated during asymmetric cell divisions in the developing mouse cortex and promotes intermediate progenitor cell fate. We carry out RNA immunoprecipitation with a Stau2 specific antibody, followed by microarray analysis to identify Stau2 assoicated RNAs that may be shuttled asymmetrically into one daughter cell thus affecting cell fate. Cortex was dissected from E13-14 timed-pregnant Swiss Webster Mice (Taconic) and RNA immunoprecipitation followed by microarray analysis was carried out to identy Stau2 associated RNA cargos.
2012-12-21 | E-GEOD-38222 | biostudies-arrayexpress
Project description:The double-stranded RNA binding protein Staufen2 (Stau2) is asymmetrically localized and segregated during asymmetric cell divisions in the developing mouse cortex and promotes intermediate progenitor cell fate. We carry out RNA immunoprecipitation with a Stau2 specific antibody, followed by microarray analysis to identify Stau2 assoicated RNAs that may be shuttled asymmetrically into one daughter cell thus affecting cell fate.
2012-12-21 | GSE38222 | GEO
Project description:Combinations of post-translational histone modifications shape the chromatin landscape during cell development in eukaryotes. However, little is known about the modifications exactly delineating functionally engaged regulatory elements. For example, although histone H3 lysine 4 mono-methylation (H3K4me1) indicates the presence of transcriptional gene enhancers, it does not provide clear-cut information about their actual position and stage-specific activity. Histone marks were, therefore, studied here at genomic loci differentially expressed in early stages of T-lymphocyte development. The concomitant presence of the three H3K4 methylation states (H3K4me1/2/3) was found to clearly reflect the activity of bona fide T-cell gene enhancers. Globally, gain or loss of H3K4me2/3 at distal genomic regions correlated with, respectively, the induction or the repression of associated genes during T-cell development. In the Tcrb gene enhancer, the H3K4me3-to-H3K4me1 ratio decreases with the enhancer’s strength. Lastly, enhancer association of RNA-polymerase II (Pol II) correlated with the presence of H3K4me3 and Pol II accumulation resulted in local increase of H3K4me3. Our results suggest the existence of functional links between Pol II occupancy, H3K4me3 enrichment and enhancer activity. ChIP-seq for H3K4me1, H3K4me3 and Pol II was performed from DRag thymocytes or DRag thymocytes from CD3 stimulated mice
2014-03-07 | E-GEOD-55635 | biostudies-arrayexpress
Project description:We performed ChIP-seq on mouse lens epithelial cells (αTN4) and mouse newborn lens. Genome-wide binding sites of Pax6, H3K4me1, H3K4me2, H3K4me3, and RNA polymerase II were generated. We also performed RNA-seq on αTN4 cells treated with Pax6 and control shRNAs.
2017-02-10 | GSE76315 | GEO
Project description:Trimethylation of histone H3 lysine 4 (H3K4me3) is associated with transcriptional start sites and proposed to regulate transcription initiation. However, redundant functions of the H3K4 SET1/COMPASS methyltransferase complexes complicate elucidation of the specific role of H3K4me3 in transcriptional regulation. Here, we show that acute ablation of shared subunits of the SET1/COMPASS complexes leads to complete loss of all H3K4 methylation. H3K4me3 turnover occurs more rapidly than H3K4me1 and H3K4me2 and is dependent on KDM5 demethylases. Surprisingly, acute loss of H3K4me3 does not have detectable effects on transcriptional initiation but leads to a widespread decrease in transcriptional output, an increase in RNA polymerase II (RNAPII) pausing and slower elongation. Our study demonstrates a distinct role for H3K4me3 in transcriptional pause-release and elongation rather than transcriptional initiation.
2023-03-14 | PXD028858 | Pride
Project description:RNA-seq on K562 cells treated with a CRISPR gRNA against STAU2. (STAU2-BGKcLV11) For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
2021-06-15 | GSE178044 | GEO