Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cis-regulatory chromatin loops analysis identifies GRHL3 as a master regulator of surface epithelium commitment

ABSTRACT: Cis-regulatory chromatin loops analysis identifies GRHL3 as a master regulator of surface epithelium commitment

PROVIDER: PRJNA1125389 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR29462250_1.fastq.gz	Fastqsanger.gz
	SRR29462250_2.fastq.gz	Fastqsanger.gz
	SRR29462251_1.fastq.gz	Fastqsanger.gz
	SRR29462251_2.fastq.gz	Fastqsanger.gz
	SRR29462252_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 32

Similar Datasets

Cis-regulatory chromatin loops analysis identifies GRHL3 as a master regulator of surface epithelium commitment

Project description:Understanding the regulatory network of cell fate acquisition remains a major challenge. Using the induction of surface epithelium (SE) from human embryonic stem cells as a paradigm, we show that the dynamic changes in morphology-related genes (MRGs) closely correspond to SE fate transitions. The marked remodeling of cytoskeleton indicates the initiation of SE differentiation. By integrating promoter interactions, epigenomic features, and transcriptome, we delineate an SE-specific cis-regulatory network and identify grainyhead-like 3 (GRHL3) as an initiation factor sufficient to drive SE commitment. Mechanically, GRHL3 primes the SE chromatin accessibility landscape and activates SE-initiating gene expression. In addition, the evaluation of GRHL3-mediated promoter interactions unveils a positive feedback loop of GRHL3 and bone morphogenetic protein 4 on SE fate decisions. Our work proposes a concept that MRGs could be used to identify cell fate transitions and provides insights into regulatory principles of SE lineage development and stem cell?based regenerative medicine.

2024-06-25 | GSE270184 | GEO

Cis-regulatory chromatin loops analysis identifies GRHL3 as a master regulator of surface epithelium commitment.

| S-EPMC9278850 | biostudies-literature

GRHL3 regulates the chromatin state during epidermal differentiation

Project description:The process of differentiation is tightly controlled, and such complex coordination of gene expression requires many layers of regulation. One such mechanism of regulation occurs through distal genomic regions called enhancers, which are believed to act as concentrating sites for transcription factors, like GRHL3, and other regulators, forming loops to contact promoters and enhance transcription. Active enhancers have been shown to have high levels of H3K4me1 and H3K27ac modified nucleosomes, with low levels of H3K4me3, while poised developmental enhancers have been shown to have H3K27me3 in place of H3K27ac. Additionally, in each cell type, a select few enhancers have been found to be unusually long (more than 12.5kb) and show high intensity of transcription factor binding and chromatin enhancer signature marks. These regions, termed super enhancers, are frequently tissue-specific and are thought to regulate the unique gene expression programs in each tissue. ChIP-Seq analysis revealed GRHL3 binding to be strongly enriched within enhancers and super enhancers in differentiating keratinocytes, however the effect of GRHL3 binding on enhancer and super enhancer activity and function is not known.

2017-04-12 | GSE76691 | GEO

Genome-wide binding of WDR5 and GRHL3

Project description:The antagonistic actions of Polycomb and Trithorax are responsible for proper cell fate determination in mammalian tissues. In the epidermis, a self-renewing epithelium, previous work has shown that release from Polycomb repression only partially explains differentiation gene activation. We now show that Trithorax is also a key regulator of epidermal differentiation, not only through activation of genes repressed by Polycomb in progenitor cells, but also through activation of genes independent of regulation by Polycomb. The differentiation associated transcription factor GRHL3/GET1 recruits the ubiquitously expressed Trithorax complex to a subset of differentiation genes. Examination of WDR5 and GRHL3 binding in human differentited primary keratinocytes (NHEK). High calcium medium was added to NHEK cells at 50% confluency to induce differentiation. Cells were collected for ChIP 24 hours after addition of high calcium medium. ChIP with Wdr5 and Grhl3 antibodies, and an input control were sequenced.

2012-11-10 | E-GEOD-42180 | biostudies-arrayexpress

Dual role of GRHL3 in bladder carcinogenesis is associated with histological subtypes

Project description:Grainyhead-like transcription factor 3 (GRHL3) is known to affect cancer development depending on subtypes in various entities. Here, we analyzed the subtype-specific role of GRHL3 in bladder carcinogenesis comparing common urothelial carcinoma (UC) with squamous bladder cancers (sq-BLCA). We examined GRHL3 mRNA and protein expression in cohorts of patient samples, its prognostic role as well as its functional impact on tumorigeneses in different molecular and histopathological subtypes of bladder cancer. We showed for GRHL3 a reverse expression in squamous and urothelial bladder cancer subtypes. Stably GRHL3 overexpressing EJ28 and SCaBER in vitro models revealed a tumor suppressive function in squamous and a oncogenic role in the urothelial cancer cells affecting cell migratory and invasive capacities. Transcriptomic profiling demonstrated highly subtype specific GRHL3 regulated expression networks coined by enrichment of genes involved in integrin mediated pathways. In SCaBER loss of RhoA GTPase activity was demonstrated associated with co-regulation of EIF4E3, a potential tumor suppressor gene. Thus, our data provide for the first time a detailed insight into the role of the transcription factor GRHL3 in different histopathological subtypes of bladder cancer.

2024-06-20 | GSE241298 | GEO

Analysis of gene expression in differentiated human primary keratinocytes depleted for Grainyhead like 3 (GRHL3)

Project description:Human primary keratinocytes were depleted of GRHL3 by siRNA and induced to differentiated for 2 days by addition of Calcium Primary normal human keratinocytes were transfected with GRHL3 or scrambled control siRNA using RNAi max (Life Technologies). 24 hours post transfection medium was raised to 1.8mM to induce differentiation. Cells were collected 48 hours later.

2012-07-18 | E-GEOD-37049 | biostudies-arrayexpress

Grhl3 is essential for epidermal barrier repair from both physical and immune injury, relevance to lesional skin disease

Project description:Epidermal barrier repair mechanisms activated in psoriasis lesions are likely involved in limiting the severity of this disease. We show that loss of grainyhead-like 3 (Grhl3), a pro-terminal differentiation factor in the epidermis, is sufficient to trigger greater sensitivity to and delayed resolution of epidermal lesions resulting from either physical or immune mediated barrier injury. After stimulation of Toll like receptors, the loss of Grhl3 resulted in increased epidermal damage with a striking increase in basal cell proliferation, hyperplasia of partially differentiated suprabasal layers, and a transcriptional profile highlighted by the overexpression of epidermal wound response and alarmin genes. This study reveals an important role for the epidermis in the initiation and recovery from immune-mediated lesions, and indicated that the epidermal regulator Grhl3 acts to both suppress disease initiation and resolve existing lesions. This work suggests that treatments focused on improving barrier function could be used preventatively and therapeutically in psoriasis. Whole skin was collected from E16.5 mouse backskins for Grhl3 ChIP. Adult epidermis for depilation and imiquimod experiments was seperated from dermis using dispase prior to Grhl3 ChIP.

2014-09-01 | E-GEOD-52648 | biostudies-arrayexpress

Differentially expressed genes in Oesophageal tumours in Grhl3 cKO mice in comparison with WT mice

Project description:RNA Seq analysis was performed on tissue from tumours from five Grhl3 knock out mice and five wild type mice treated with 4-NQO to determine the effect of 4-NQO exposure to the oseophagus on tumour formation in the context of Grhl3 knockout. Tissue were excised and microdissected for RNA Seq analysis.

2020-11-01 | GSE122175 | GEO

GRHL3 activates FSCN1 to relax cell adhesions between migrating keratinocytes in the wound front

Project description:identify an underlying mechanism a new pathway where GRHL3 activates the Fscn1 gene to effect cell-cell loosening in the migrating wound front

2021-10-13 | GSE172161 | GEO

Analysis of gene expression in differentiated human primary keratinocytes depleted for Grainyhead like 3 (GRHL3)

Project description:Human primary keratinocytes were depleted of GRHL3 by siRNA and induced to differentiated for 2 days by addition of Calcium

2012-07-19 | GSE37049 | GEO