Similar Datasets
Project description:Genome-wide maps of SNIP1 in 293T
| PRJNA486842 | ENA
Project description:In this project, we performed DPF3 and SNIP1 immunoprecipitation followed by mass spectrometry analysis to identify their interacting partners.
2022-08-22 | PXD033421 | Pride
Project description:RNAseq was performed on brain cells conditionally depleted from Snip1, and the PRC2 subunit Eed.
2023-07-12 | GSE212103 | GEO
Project description:Splicing Factor 3b Subunit 1 (SF3B1), a core component of the spliceosome, undergoes dynamic phosphorylation and dephosphorylation during the splicing cycle to regulate pre-mRNA splicing. Twenty-eight threonine/proline repeats are phosphorylated by CDK11 during spliceosome activation and remain phosphorylated in the catalytically active spliceosomes. The function of phosphorylated SF3B1 (P-SF3B1), and the identity of spliceosomes stalled by CDK11 inhibition remain unclear. Using quantitative proteomics of chromatin-associated spliceosomes, we identify a previously uncharacterized intermediate complex BOTS964, arrested by CDK11 inhibitor OTS964, that incorporates the nineteen-related (NTR) but not nineteen (NTC) complex. iCLIP-seq revealed that P-SF3B1 engages with the U6 snRNA internal stem-loop (ISL), suggesting a potential role in stabilizing the RNA catalytic core. We further demonstrate that P-SF3B1 is recognized by forkhead-associated (FHA) domain of SNIP1, which promotes recruitment of retention and splicing (RES) complex during spliceosome activation. Acute SNIP1 depletion disrupts RES incorporation, causes widespread splicing defects, and promotes hyperphosphorylation of SF3B1 by CDK11. Mutations in SNIP1 FHA domain, including the neurodevelopmental disorder associated E366G variant, impair P-SF3B1 binding, pre-mRNA splicing, and cell viability. Together, these findings uncover the phosphorylation-dependent CDK11/P-SF3B1/SNIP1 signaling axis that is critical for pre-mRNA splicing and cellular proliferation and provide a mechanistic insight into its dysregulation in disease.
2026-02-24 | GSE295435 | GEO
Project description:Splicing Factor 3b Subunit 1 (SF3B1), a core component of the spliceosome, undergoes dynamic phosphorylation and dephosphorylation during the splicing cycle to regulate pre-mRNA splicing. Twenty-eight threonine/proline repeats are phosphorylated by CDK11 during spliceosome activation and remain phosphorylated in the catalytically active spliceosomes. The function of phosphorylated SF3B1 (P-SF3B1), and the identity of spliceosomes stalled by CDK11 inhibition remain unclear. Using quantitative proteomics of chromatin-associated spliceosomes, we identify a previously uncharacterized intermediate complex BOTS964, arrested by CDK11 inhibitor OTS964, that incorporates the nineteen-related (NTR) but not nineteen (NTC) complex. iCLIP-seq revealed that P-SF3B1 engages with the U6 snRNA internal stem-loop (ISL), suggesting a potential role in stabilizing the RNA catalytic core. We further demonstrate that P-SF3B1 is recognized by forkhead-associated (FHA) domain of SNIP1, which promotes recruitment of retention and splicing (RES) complex during spliceosome activation. Acute SNIP1 depletion disrupts RES incorporation, causes widespread splicing defects, and promotes hyperphosphorylation of SF3B1 by CDK11. Mutations in SNIP1 FHA domain, including the neurodevelopmental disorder associated E366G variant, impair P-SF3B1 binding, pre-mRNA splicing, and cell viability. Together, these findings uncover the phosphorylation-dependent CDK11/P-SF3B1/SNIP1 signaling axis that is critical for pre-mRNA splicing and cellular proliferation and provide a mechanistic insight into its dysregulation in disease.
2026-02-24 | GSE295433 | GEO
Project description:We found the genome-wide co-localization of Qki-5 and Srebp2. Notably, the genomic distribution analysis revealed that Qki-5 and Srebp2 highly co-occupied the regions of the promoter/transcription start site (TSS), where active transcription was taken place in a oligodendrocyte-specific manner, which was indicated by Pol II binding events. GO analysis of the genes whose promoters were co-bound by Qki-5, Srebp2, and Pol II showed a significant enrichment of the Srebp2-mediated cholesterol biosynthesis pathway, and Qki depletion led to reduced recruitment of Srebp2 and Pol II on the promoters of the genes involved in cholesterol biosynthesis. These data suggest Qki-5 as a potential transcription co-activator of Srebp2-mediated cholesterol biosynthesis in oligodendrocytes.
2021-05-10 | GSE144756 | GEO
Project description:We found that there is a big overlap between the Qki5- and PPARb-binding events by ChIP-seq. Interestingly, the genomic distribution analyses of Qki-5- and PPARβ-binding events showed significant enrichment at the regions of the promoter/transcription start site (TSS) which were indicated by Pol II-binding events. The strong preference of the promoter/TSS co-occupancy suggested that Qki-5 might play an important role in PPARβ-mediated transcriptional regulation of its downstream genes.
2020-01-05 | GSE126577 | GEO
Project description:We used chromatin immunoprecipitation (ChIP) in combination with human promoter microarrays to idnetify SUZ12 and H3K27me3-occupied gene promoters in prostate cancer cells and tissues. We observed a common set of SUZ12 and H3K27me3-occupied genes in LNCaP cells, and metastatic prostate cancer tissues across individuals as well as tissue types of the metastatic sites. We also found significant overlap of cancer polycomb targets with previously published embryonic stem cell polycomb targets. In addition, a strong association between cancer polycomb targets with prostate cancer outcome was observed. We developed a cancer Polycomb Repression Signature, comprised direct targets of PRC2 silencing in cancer, that is predictive of cancer outcome in multiple expression profling datasets of tumors. Keywords: protein-DNA interaction
2007-11-01 | GSE9069 | GEO
Project description:The discovery of cytosine hydroxymethylation (5-hmC) as a mechanism that potentially controls DNA methylation changes typical of neoplasia prompted us to investigate its behavior in colon cancer. 5-hmC is globally reduced in proliferating cells such as colon tumors and the gut crypt progenitors, from which tumors can arise. Here, we show that colorectal tumors and cancer cells express Ten-Eleven Translocation (TET) transcripts at levels similar to normal tissues. Genome-wide analyses show that promoters marked by 5-hmC in normal tissue, and those identified as TET2 targets in colorectal cancer cells, are resistant to methylation gain in cancer. In vitro studies of TET2 in cancer cells confirm that these promoters are resistant to methylation gain independently of sustained TET2 expression. We also find that a considerable number of the methylation gain-resistant promoters marked by 5-hmC in normal colon overlap with those that are marked with poised bivalent histone modifications in embryonic stem cells. Together our results indicate that promoters that acquire 5-hmC upon normal colon differentiation are innately resistant to neoplastic hypermethylation by mechanisms that do not require high levels of 5-hmC in tumors. Our study highlights the potential of cytosine modifications as biomarkers of cancerous cell proliferation. Six samples were analyzed. 2 biological replicates each of HCT116 cells stably transfected with an empty vector control (TET_KD_Plk), with shRNA to TET2 (TET_KD_2C) and with shRNA to TET2 and TET3 (TET_KD_2.3)
2015-02-03 | E-GEOD-63421 | biostudies-arrayexpress
Project description:The discovery of cytosine hydroxymethylation (5-hmC) as a mechanism that potentially controls DNA methylation changes typical of neoplasia prompted us to investigate its behavior in colon cancer. 5-hmC is globally reduced in proliferating cells such as colon tumors and the gut crypt progenitors, from which tumors can arise. Here, we show that colorectal tumors and cancer cells express Ten-Eleven Translocation (TET) transcripts at levels similar to normal tissues. Genome-wide analyses show that promoters marked by 5-hmC in normal tissue, and those identified as TET2 targets in colorectal cancer cells, are resistant to methylation gain in cancer. In vitro studies of TET2 in cancer cells confirm that these promoters are resistant to methylation gain independently of sustained TET2 expression. We also find that a considerable number of the methylation gain-resistant promoters marked by 5-hmC in normal colon overlap with those that are marked with poised bivalent histone modifications in embryonic stem cells. Together our results indicate that promoters that acquire 5-hmC upon normal colon differentiation are innately resistant to neoplastic hypermethylation by mechanisms that do not require high levels of 5-hmC in tumors. Our study highlights the potential of cytosine modifications as biomarkers of cancerous cell proliferation. 5 normal colon samples and 4 matching tumor samples were profiled for 5-hydroxymethylcytosine content genomewide using hmeDIP-seq. The colorectal cancer cell line HCT116 was profiled for binding of TET2 genomewide by chromatin immunoprecipitation sequencing (ChIP-seq).
2015-02-03 | E-GEOD-47590 | biostudies-arrayexpress