Similar Datasets
Project description:Nascent RNA sequencing of FOXD3 KO and WT mouse ESCs
| PRJNA760650 | ENA
Project description:We performed CUT&Tag of inducible FOXD3 KO cells with or without cell cycle phase sorting to determine impact of FOXD3 loss of active chromatin marks.
2023-04-30 | GSE183419 | GEO
Project description:We performed ATAC seq of inducible FOXD3 KO cells after cell cycle phase sorting to determine impact of FOXD3 loss on chromatin accessibility.
2023-04-30 | GSE183417 | GEO
Project description:We performed streptavidin pulldown sequencing of endogenously and exogenously Avi-tagged FOXD3 to determine genome-wide binding pattern of this transcription factor in asynchronous or cell cycle synchronized naive mouse ESCs.
2023-04-30 | GSE183418 | GEO
Project description:Transcription factor/enhancer interactions determine cell specific gene expression. Here, we followed enhancers during differentiations of embryonic stem (ESCs) to epiblast like cells (EpiLCs). There were highly dynamic changes in histone lysine 27 acetylation at enhancer sites throughout the genome. These sites were enriched for a Foxd3 binding motif, a forkhead transcription factor essential in early embryonic development. Surprisingly, Foxd3 occupied largely mutually exclusive sites in the ESCs versus EpiLCs. Foxd3 bound to nucleosome occupied regions, simultaneously evicting the histones while inhibiting full gene expression through the recruitment of histone deacetylases. Knockout of Foxd3 resulted in hyperacetylation and transcriptional upregulation of neighboring genes, many of which were further upregulated at later stages of differentiation. These data show that Foxd3 primes enhancer sites during pregastrulation by removing nucleosomes, yet suppresses neighboring histone hyperacetylation. Such a mechanism may be common to many transcription factors that prepare enhancers for later gene activation during development. ChIP-seq of H3K4me1, H3K27ac, H3K27me3, p300, H3K4me3, RNA Pol2 and Oct4 in four pluripotent states: embryonic stem cells (ESCs) day 1 ESC differentiation, Epi-like stem cells (EpiLCs), and epiblast stem cells (EpiSCs); ChIP-seq of 3XFlag tagged Foxd3 in ESCs and EpiLCs; ChIP-seq of H3K4me1, H3K27ac, H3K27me3, p300 and H3K4me3 in Foxd3 conditional knockout cells (tamoxifen-inducible) -/+ 36h Tamoxifen treatemnt. ChIP seq of Flag-Foxd3 (third replicate), ChIP-seq of HDAC1 and Brg1 in WT and Foxd3 KO cells and MNase-ChIP-seq of H3K4me1
2015-12-08 | E-GEOD-58407 | biostudies-arrayexpress
Project description:FOXD3 is essential in embryonic stem cells, however the primary molecular mechanism is unclear. Here, we performed BioID to identify proteins collaborating with FOXD3 in protecting embryonic stem cell survival.
2023-05-08 | PXD035284 | Pride
Project description:Genome-wide binding of FOXD3 in mouse ESCs
| PRJNA760537 | ENA
Project description:The transcription factor forkhead box D3 (FoxD3) is a transcriptional factor which belongs to forkhead box (Fox) transcription factor family. The functions of FOXD3 in embryogenesis and in the development of neural crest cells have been clearly defined. Its tumor suppressor function hasbeen found in many types of cancer in recent years. However, the study about its roles in lung cancerdevelopment is still lacking. Our study found that deficiency of FoxD3 in lung cancer enhanced cell growth and cell invasion. RNA-sequence analysis demonstrated that loss of FoxD3 mainly affected cell cycle progression related gene expression. Knockdown of FoxD3 led to G2-M cell accumulation with up-regulation of DNA replication licensing factor MCM5 and MCM4 as well as cell cycle regulator polo-like kinase-1 (PLK1) and CDC6. Over-expression of those genesin lung cancer was associated with poor clinical outcomes of lung cancer patients. We also identified high mobility group box-1(HMGB1), Hras and Ephrin B1 gene expression increase after FoxD3 silencing which may participate in enhanced lung cancer cell invasion. Our study identifiedtumor suppressor function of FoxD3 in lung cancer andwe did the first comprehensive analysis of the genes regulated by FoxD3 for cell proliferation and invasion in lung cancer. The identified genes regulated by FoxD3 through our analysis will provide valuable information to uncover the mechanism of FoxD3 tumor suppressor function.
2015-12-24 | GSE64513 | GEO
Project description:The tumor-initiating cells (TIC) are cell population that can initiate tumor, mediate drug resistance, and give rise to metastasis. FOXD3 is a forkhead box (Fox) transcription factor family that regulates the pluripotency of embryonic stem cell and tumorigenicity. However, it is unclear whether FOXD3 play any role in TIC and tumor metastasis. Here, we report that FOXD3 is down-regulated in tumor initiating cells and negatively correlated with higher histologic grades and positive lymph node metastasis. FOXD3 repress TIC expansion, cell migration, drug resistance and osteogenesis in vitro and in vivo. Mechanically, we found that FOXD3 repress a cohort of genes including SET and WDR5 and to regulate several TIC related signaling pathway. Moreover, SET and WDR5 was positively correlated with the CSC abundance and tumor progression. Besides, patients with high expression of SET and WDR5 presented a poorer overall survival. Collectively, our work defined that FOXD3-WDR5-SET axis that repress TIC accumulation and lung cancer progression.
2017-01-10 | GSE93323 | GEO
Project description:The transcription factor forkhead box D3 (FoxD3) is a transcriptional factor which belongs to forkhead box (Fox) transcription factor family. The functions of FOXD3 in embryogenesis and in the development of neural crest cells have been clearly defined. Its tumor suppressor function hasbeen found in many types of cancer in recent years. However, the study about its roles in lung cancerdevelopment is still lacking. Our study found that deficiency of FoxD3 in lung cancer enhanced cell growth and cell invasion. RNA-sequence analysis demonstrated that loss of FoxD3 mainly affected cell cycle progression related gene expression. Knockdown of FoxD3 led to G2-M cell accumulation with up-regulation of DNA replication licensing factor MCM5 and MCM4 as well as cell cycle regulator polo-like kinase-1 (PLK1) and CDC6. Over-expression of those genesin lung cancer was associated with poor clinical outcomes of lung cancer patients. We also identified high mobility group box-1(HMGB1), Hras and Ephrin B1 gene expression increase after FoxD3 silencing which may participate in enhanced lung cancer cell invasion. Our study identifiedtumor suppressor function of FoxD3 in lung cancer andwe did the first comprehensive analysis of the genes regulated by FoxD3 for cell proliferation and invasion in lung cancer. The identified genes regulated by FoxD3 through our analysis will provide valuable information to uncover the mechanism of FoxD3 tumor suppressor function. Three control and three FOXD3 knockdown A549 cell lines were subjected to RNA sequencing.
2015-12-24 | E-GEOD-64513 | biostudies-arrayexpress