Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA147227 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Cytokine treated normal human epidermal keratinocytes
| PRJNA98301 | ENA
Project description:<p>Transcription factor p63 is a key regulator of epidermal keratinocyte proliferation and differentiation. Mutations in the p63 DNA-binding domain are associated with Ectrodactyly Ectodermal Dysplasia Cleft Lip/Palate (EEC) syndrome. Underlying molecular mechanism of these mutations however remain unclear. Here we characterized the transcriptome and epigenome of p63 mutant keratinocytes derived from EEC patients. The transcriptome of p63 mutant keratinocytes deviated from the normal epidermal cell identity. Epigenomic analyses showed an altered enhancer landscape in p63 mutant keratinocytes contributed by loss of p63-bound active enhancers and by unexpected gain of enhancers. The gained enhancers were frequently bound by deregulated transcription factors such as RUNX1. Reversing RUNX1 overexpression partially rescued deregulated gene expression and the altered enhancer landscape. Our findings identify an unreported disease mechanism whereby mutant p63 rewires the enhancer landscape and affects epidermal cell identity, consolidating the pivotal role of p63 in controlling the enhancer landscape of epidermal keratinocytes.</p>
| phs001737 | dbGaP
Project description:Normal human epidermal keratinocytes (NHEK) from neonatal foreskin were cultured in serum-free EpiLife medium with human KC growth supplement (0.2% bovine pituitary extract (v/v), 5ug bovine insulin, 5ug/ml bovine transferrin, 0.5ng/ml human EGF, and 0.18 ug/ml hydrocortisone) from Cascade Biologics. Cultures were treated with recombinant cytokines from R&D Systems. J Immunol. 2007 Feb 15;178(4):2229-40. Keywords: cytokine response
2007-03-09 | GSE7216 | GEO
Project description:Normal Human Epidermal Keratinocytes treated with either Q-VD-OPh or vehicle,were prepared for protein analysis using proteomics approach.Protein expression changes were discussed.
2025-02-11 | PXD036948 | Pride
Project description:The epidermis, the most superficial layer of human skin, serves a critical barrier function, protecting the body from external pathogens and allergens. Dysregulation in the epidermal differentiation process contributes to barrier dysfunction and is implicated in the pathology of various dermatological diseases, including atopic dermatitis (AD). Mucopolysaccharide polysulfate (MPS) is used as a moisturizing agent for xerosis in AD patients. However, its mechanism of action on keratinocytes, the main constituent of the epidermis, remains unclear. In this study, we investigated the impact of MPS on keratinocytes by subjecting adult human epidermal keratinocyte (HEKa) cells and three-dimensional cultured keratinocytes to MPS treatment, followed by transcriptome analysis. The analysis revealed that MPS treatment enhances keratinocyte differentiation and suppresses proliferation. We focused on amphiregulin (AREG), a membrane protein that belongs to the epidermal growth factor (EGF) family and possesses a heparin-binding domain, as a significant target of the MPS among the genes altered by MPS. It is revealed that MPS exerts an inhibitory effect directly on AREG, rather than on the EGF receptor or other members of the EGF family. Furthermore, it is suggested that AREG leads to a reduction in epidermal barrier function, whereas MPS contributes to barrier enhancement through AREG inhibition. Collectively, these findings suggest that MPS modulates barrier function through the inhibition of AREG, offering insights into potential therapeutic strategies for skin barrier restoration.
2024-07-03 | GSE268656 | GEO
Project description:Normal human epidermal keratinocytes (NHEK) from neonatal foreskin were cultured in serum-free EpiLife medium with human KC growth supplement (0.2% bovine pituitary extract (v/v), 5ug bovine insulin, 5ug/ml bovine transferrin, 0.5ng/ml human EGF, and 0.18 ug/ml hydrocortisone) from Cascade Biologics. Cultures were treated with recombinant cytokines from R&D Systems. J Immunol. 2007 Feb 15;178(4):2229-40. Experiment Overall Design: NHEK were treated with IL-19, IL20, IL-22, and IL24, with controls untreated, along with IL1b, IFN gamma, and KGF.
2007-11-01 | E-GEOD-7216 | biostudies-arrayexpress
Project description:Gene expression profile of normal human epidermal keratinocytes treated with adenosine
2021-01-22 | GSE165222 | GEO
Project description:It has long been known that excessive mitotic activity due to H-Ras can block keratinocyte differentiation and cause skin cancer. It is not clear, however, whether there are any innate surveillants that ensure keratinocytes undergoing terminal differentiation, preventing the disease. IKKα induces keratinocyte terminal differentiation and its reduction promotes skin tumor development. However, its nature function in skin cancer is unknown. Here we found that mice with IKKα deletion in keratinocytes or in hair follicle keratinocytes developed a thickened epidermis and spontaneous squamous cell-like carcinomas. Inactivation of epidermal growth factor receptor (EGFR) or reintroduction of IKKα inhibited excessive mitosis, induced terminal differentiation, and prevented skin cancer through an EGFR-driven autocrine loop in mice. Thus, IKKα serves as an innate surveillant. Experiment Overall Design: The differences in gene expression profiles of CHUK deleted mouse keratinocytes compared to wild type mouse keratinocytes were analyzed using two dual-channel agilent microarrays in duplicates.
2009-08-12 | E-GEOD-12111 | biostudies-arrayexpress
Project description:Epidermal growth factor (EGF) is a potent mitogenic agent promoting cell differentiation, proliferation, and growth. The kidney thick ascending limb of Henle’s loop and distal convoluted tubule were identified as major sites of EGF synthesis. As expected, EGF can modulate the functioning of kidney collecting duct including osmotic water permeability (Pf). Here, we found that EGF (0.1 uM) reduced the vasopressin-stimulated Pf by 26% in isolated perfused rat inner medullary collecting duct (IMCD). Immunoblotting using IMCD suspensions prepared in similar condition showed that EGF significantly reduced phosphorylation of AQP2 at Ser264 and Ser269 but had not affected on Ser256 or proline-directed Ser261 site. Quantitative phosphoproteomics was carried out to investigate other effects of EGF. Rat IMCD suspensions were treated with 1 M of EGF or vehicle for 30 min. Samples from three replicates of experiment were analyzed by TMT isobaric labeling quantitative protein mass spectrometry. We identified 23859 phosphopeptides with unique phosphorylation sites in EGF-treated rat IMCD samples, with 25 proteins increased and 100 proteins decreased in phosphorylation as determined by dual statistical analysis. EGF induced phosphorylation of multiple residues at the C-terminus of EGF receptor, EGFR or Erbb1, and mildly activated the classical MAPK pathway, RAF-MEK-ERK. EGF also affected phosphorylation of several proteins in PI3K/Akt pathway involved in cap-dependent translation initiation (Eif4ebp1, Gigyf2, Eif3b, Eif4g3, Pdcd4) and translation elongation (Eef2k, Eef2), predicted an overall translation repression. In comparison with a dDAVP-induced phosphoproteome, we found that the majority of proteins had phosphorylation change on specific site by either EGF or dDAVP but not both, suggesting a highly selectivity of phosphorylation modification induced by these two agents. Among the 25 peptides that had phosphorylation change on the same site by both EGF and dDAVP, AQP2 at Ser264/Ser269 was changed in opposite direction. We concluded that the short-term effect of EGF is insufficient to cause an effect on Ser261 phosphorylation of AQP2 in normal rat IMCD.
2025-06-26 | PXD017192 | Pride
Project description:Our aim was to investigate the interaction between epidermal differentiation and VZV infection. By means of a calcium-induced keratinocyte differentiation model and RNA-seq we show VZV infection has a profound effect on differentiating keratinocytes and hijacks the normal process of epidermal gene expression to generate a signature resembling patterns of gene expression seen in both heritable and acquired skin-blistering disorders. Analysis of the viral transcriptome provides evidence that VZV replication in skin is tightly linked to differentiation and critically, that late viral gene expression is associated with cellular differentiation. The experiment was performed on human primary keratinocytes under four conditions: undifferentiated/uninfected, uninfected/differentiated, VZV-infected/undifferentiated and VZV-infected/differentiated.
2014-05-29 | E-MTAB-1717 | biostudies-arrayexpress