Similar Datasets
Project description:c-Jun binding profile in Cal-33 cells
| PRJNA986182 | ENA
Project description:The somatic cell fate can be converted to tumor or pluripotent ones by ectopic expression of transcription factors in vitro and in vivo. Many oncogenic transcription factors are known to mediate both fates as they share similar proliferative and metabolic properties. Paradoxically, we found c-Jun as the first oncogene that appears to specify a somatic fate, oppose the pluripotent one and impede reprogramming. We performed a series of high through out sequencing to understand the way cJun works. To understand how c-Jun drives mESCs differentiating, we obtained c-Jun TetOn mESCs, and performed RNAseq 36h later with dox inducing or not . To understand why c-Jun blocks reprogramming while c-JunDN and Jdp2 can replace Oct4, we overexpressed these factors with KSM during reprogramming and performed RNAseq 3 Days after virus transfection. Moreover, to extend understand how these factors regulate gene expression, we also overexpressed these factors in MEF and performed RNAseq. Further more, to understand how cJun regulates cell fates and gene expression, we overexpressed c-Jun in mouse ESC and performed ChIP-seq. Also, we performed c-JunDN ChIP-seq during somatic cells reprogramming on day 3, to explore the binding sites of c-JunDN.
2015-06-10 | E-GEOD-50776 | biostudies-arrayexpress
Project description:We report the genome-wide profile of cJun and p27 in _231 (a line selected for low metastatic ability), _231-1833 (its bone-tropic metastatic derivative line), _231p27CK-DD (a phosphomimetic cell line), and _231-1833shp27 (p27 knockdown cell line). It shows that cJun and p27 broadly binds to genomic DNA and their bindings are regulated by p27 phosphorylation-dependent patterns.
2019-03-19 | GSE112444 | GEO
Project description:Focal adhesion kinase (FAK) localizes to focal adhesions and is overexpressed in many cancers. FAK can also translocate to the nucleus, where it binds to, and regulates, several transcription factors, including MBD2, p53 and IL-33, to control gene expression by unknown mechanisms. We have used ATAC-seq to reveal that FAK controls chromatin accessibility at a subset of regulated genes. Integration of ATAC-seq and RNA-seq data showed that FAK-dependent chromatin accessibility is linked to differential gene expression, including of the FAK-regulated cytokine and transcriptional regulator interleukin-33 (Il33), which controls anti-tumor immunity. Analysis of the accessibility peaks on the Il33 gene promoter/enhancer regions revealed sequences for several transcription factors, including ETS and AP-1 motifs, and we show that c-Jun, a component of AP-1, regulates Il33 gene expression by binding to its enhancer in a FAK kinase-dependent manner. This work provides the first demonstration that FAK controls transcription via chromatin accessibility, identifying a novel mechanism by which nuclear FAK regulates biologically important gene expression.
| S-EPMC7794255 | biostudies-literature
Project description:Study was conducted to understand the effect of the cancer associated H2BG53D mutation in PDAC. Using CRISPR/Cas9 Knock-in cell lines expressing FLAG-tagged WT and G53D mutant H2B, we conducted gene expression profilling experiments and studied the effect of the H2BG53D mutation on transcription and PDAC development.
2020-07-01 | GSE134864 | GEO
Project description:Apoptotic neuron death is a common feature of many neurodegenerative diseases. Perhaps surprisingly, the exact mechanisms by which neurons undergo apoptosis have yet to be elucidated. We conducted an unbiased whole genome screen in human neurons to discover genes required for apoptotic neuron death, and found ATF2, MAP3K12 and JUN among top hits. We demonstrate that ATF2 is a previously unappreciated master regulator of neuron death. ATF2 is phosphorylated downstream of MAP3K12 (dual leucine zipper kinase) and MAP3K13 (leucine zipper kinase) and its phosphorylation is essential for transcriptional upregulation of JUN. We show that JUN upregulation is essential for apoptosis – but not its phosphorylation. Contrary to previous assumptions, cJun phosphorylation is therefore simply a correlate of JUN upregulation. In this study, we identify phosphorylation of ATF2 as a key event in the mechanism of neuronal apoptosis, linking the MAP3K12/13 kinase cascade to transcriptional upregulation of JUN. Since targeting members of this signaling pathway to block neuronal death has proved difficult, ATF2 offers a novel and promising alternative.
2025-04-30 | GSE282354 | GEO
Project description:STAT1 is the major transcription factor (TF) driving response to exposure to IFNg. C-JUN is a TF which has been shown to bind with STAT1 and act as a partner TF. We have expression profiled WT and CJUN-/- MEFs in order to determine the set of IFNg genes regulated by STAT1 and C-JUN. This study was designed primarily to test the accuracy of in silico cis-regulatory module prediction algorithm called SCRM. The set of genes differentially expressed after IFNg are likely to be targets of the TF STAT1. A subset of these genes will also be targeted by partner TFs of STAT1 (e.g. C-JUN). By measuring the expression of the WT IFNg responsive genes in a C-JUN-/- model, the subset of genes that are regulated by C-JUN can be ascertained. This set of genes can then be compared against those predicted to be regulated by C-JUN using the in silico approach SCRM, and therefore the accuracy of the in silico predictions can be determined.
2012-03-20 | GSE26205 | GEO
Project description:We conducted gene expression profilling of common prostate cell lines for comparison with genome-wide DNA methylation profiles for the same cell lines to study the impact of differential DNA methylation in prostate cancer.
2012-12-19 | GSE35401 | GEO
Project description:In mammalian cells, 5-methylcytosine (5mC) occurs in genomic double-stranded DNA (dsDNA) and is enzymatically oxidized to 5-hydroxymethylcytosine (5hmC), then to 5-formylcytosine (5fC), and finally to 5-carboxylcytosine (5caC). These cytosine modifications are enriched in regulatory regions of the genome. The effect of these oxidative products on five bZIP dimers (CREB1, ATF2, Zta, ATF3|cJun, and cFos|cJun) binding to five types of dsDNA was measured using protein binding microarrays. The five dsDNAs contain either cytosine in both DNA strands or cytosine in one strand and either 5mC, 5hmC, 5fC, or 5caC in the second strand. Some sequences containing the CEBP half-site GCAA are bound more strongly by all five bZIP domains when dsDNA contains 5mC, 5hmC, or 5fC. dsDNA containing 5caC in some TRE (AP-1)-like sequences, e.g., TGACTAA, is better bound by Zta, ATF3|cJun, and cFos|cJun.
2020-11-16 | GSE141050 | GEO
Project description:The somatic cell fate can be converted to tumor or pluripotent ones by ectopic expression of transcription factors in vitro and in vivo. Many oncogenic transcription factors are known to mediate both fates as they share similar proliferative and metabolic properties. Paradoxically, we found c-Jun as the first oncogene that appears to specify a somatic fate, oppose the pluripotent one and impede reprogramming. We performed a series of high through out sequencing to understand the way cJun works.
2015-06-10 | GSE50776 | GEO