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Krüppel-like factor 5 rewires NANOG regulatory network to activate human morulablastocyst specific LTR7Y and promote naïve pluripotency [CUT&Tag]

ABSTRACT: Genomic profiling of NANOG binding in KLF4 KLF5 double knockouts naïve human embryonic stem cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE190882 | GEO | 2022/08/27

REPOSITORIES: GEO

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Krüppel-like factor 5 rewires NANOG regulatory network to activate human morulablastocyst specific LTR7Y and promote naïve pluripotency [ChIP-seq]

Project description:We report the genomic binding profile of KLF5, NANOG and H3K27ac in human naïve ESCs

2022-08-27 | GSE169673 | GEO

Krüppel-like factor 5 rewires NANOG regulatory network to activate human morulablastocyst specific LTR7Y and promote naïve pluripotency [RNA-seq]

Project description:Transcriptome profiling for KLF4 and/or KLF5 knockout lines in human naïve embryonic stem cells Transcriptome profiling for CRISPRa-LTR7Y or KLF5 overexpression in primed human embryonic stem cells

2022-08-27 | GSE169675 | GEO

Krüppel-like factor 5 rewires NANOG regulatory network to activate human morulablastocyst specific LTR7Y and promote naïve pluripotency [ATAC-seq]

Project description:ATAC-seq profiling and comparison for chromatin accessibility in human primed embryonic stem cells (ESCs), primed ESCs overexpressing KLF5, and naïve ESCs.

2022-08-27 | GSE169671 | GEO

Krüppel-like factor 5 rewires NANOG regulatory network to activate human morulablastocyst specific LTR7Y and promote naïve pluripotency

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

2022-08-27 | GSE169678 | GEO

Krüppel-like factor 5 rewires NANOG regulatory network to activate human morulablastocyst specific LTR7Y and promote naïve pluripotency [scRNA-seq]

Project description:Single cell transcriptome profiling of human naïve embryonic stem cells.

2022-08-27 | GSE207431 | GEO

Krüppel-Like Factor 5 Regulates Airway Epithelial Cell Identity and Function [RNA-seq]

Project description:A complex network of transcription factors regulates genes involved in establishing and maintaining key biological properties of the human airway epithelium. Here we characterize the role of Krüppel-Like Factor 5 (KLF5), in controlling essential pathways of epithelial cell identity and function in the human lung. RNA-seq following siRNA-mediated depletion of KLF5 in the Calu-3 lung epithelial cell line identified significant enrichment of genes encoding chemokines and cytokines involved in the proinflammatory response, and also components of the junctional complexes mediating cell adhesion. To determine direct gene targets of KLF5, we defined the cistrome of KLF5 using ChIP-seq in both Calu-3 and 16HBE14o- lung epithelial cells lines. Occupancy site concordance analysis revealed that KLF5 co-localized with the active histone modification H3K27ac and also with binding sites for CCAAT Enhancer Binding Protein Beta (C/EBPβ). Depletion of KLF5 increased both the expression and secretion of important chemokines, a response that was enhanced following exposure to Pseudomonas aeruginosa lipopolysaccharide. Wound scratch assays in Calu-3 cells exhibited faster rates of repair after KLF5 depletion than did negative controls. Similarly, CRISPR-mediated KLF5-null 16HBE14o- cells also showed enhanced wound closure. These data reveal a pivotal role for KLF5 in coordinating epithelial functions relevant to human lung disease.

2021-10-07 | GSE164851 | GEO

Krüppel-Like Factor 5 Regulates Airway Epithelial Cell Identity and Function [CHIP-seq]

2021-10-07 | GSE164852 | GEO

Gene expression signatures for Nanog-positive and Nanog-negative hepatocellular carcinoma cells

Project description:Whole genome microarray expression profiling of HCC cell line (Huh7) and patients derive primary HCC cells (T1115 and T1224) expressing Nanog or not. Results provide insight into the role of Nanog in transcriptional regulation.

2014-11-13 | GSE33741 | GEO

Nanog-induced intestinal and colonic hyperplasia

Project description:Though expression of the homeobox transcription factor Nanog is generally restricted to pluripotent cells and early germ cells, recent reports have found that Nanog is re-expressed in somatic and germ cell tumors associated with poor differentiation and aggressive disease progression. To elucidate its oncogenic properties, a modified Tet-On system was utilised to generate Nanog-inducible mice. By dexamethasone and doxycycline injection, similar Nanog expression levels as in wild-type embryonic stem cells were obtained in all major organs except for brain. Ectopic Nanog expression resulted in intestinal and colonic epithelium hyperplasia-intestinal villi had doubled in length and hyperplastic epithelium outgrowths were seen after 7 days. The tumor suppressor gene Cdx2 was downregulated at onset of Nanog expression, suggesting that crosstalk between Nanog and Cdx2 is conserved from early embryo development to adulthood. Although the mice died before they could form tumors, Cdx2 repression and intestinal hyperplasia links Nanog to tumor initiation.

2014-08-11 | GSE31413 | GEO

Defining a critical Nanog enhancer using chromatin-focused approaches identifies RNAPII recruitment as required for expression [CUT&Tag]

Project description:Transcriptional enhancers have been defined by their ability to operate independent of distance and orientation in plasmid reporters rather than native chromatin. We employed a combination of approaches to investigate the Nanog locus in mouse embryonic stem cells (ESCs) and an associated cis regulatory element (CRE) which may operate as either a super-enhancer (SE) or alternative promoter. We establish this element is a SE within chromatin using distance- and orientation-independence as criteria, and that it regulates Nanog by recruiting and/or initiating RNA Polymerase II. Our work highlights that enhancers can regulate gene expression through a diverse set of mechanisms.

2020-12-07 | GSE143991 | GEO

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