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Gene expression data of fibroblasts transduced with LacZ or p63+KLF4.

ABSTRACT: To determine if fibroblasts could be reprogrammed to a keratinocyte phenotype p63+KLF4 or LacZ expressing retroviruses were transduced into primary human neonatal fibroblasts. Global gene expression profiling using U133 plus 2.0 arrays were used to deteremine the extent of reprogramming to a keratinocyte phenoypte upon transduction with p63+KLF4. Fibroblasts transduced with p63+KLF4 were also treated +/- high calcium to determine if treatment with calcium could induce differentiation of these cells. Microarray analysis was also performed on cells treated +/- calcium.

ORGANISM(S): Homo sapiens

PROVIDER: GSE47746 | GEO | 2013/11/03

SECONDARY ACCESSION(S): PRJNA207551

REPOSITORIES: GEO

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Gene expression data of fibroblasts transduced with LacZ or p63+KLF4.

Project description:To determine if fibroblasts could be reprogrammed to a keratinocyte phenotype p63+KLF4 or LacZ expressing retroviruses were transduced into primary human neonatal fibroblasts. Global gene expression profiling using U133 plus 2.0 arrays were used to deteremine the extent of reprogramming to a keratinocyte phenoypte upon transduction with p63+KLF4. Fibroblasts transduced with p63+KLF4 were also treated +/- high calcium to determine if treatment with calcium could induce differentiation of these cells. Microarray analysis was also performed on cells treated +/- calcium. For gene expression profiling, cultured human fibroblasts were infected with LacZ or p63+KLF4 expressing retroviruses. p63+KLF4 cells were also treated +/- calcium. Microarray analysis using Affymetrix HG-U133 2.0 plus arrays was performed on duplicate samples.

2013-11-03 | E-GEOD-47746 | biostudies-arrayexpress

Homo sapiens

Project description:Gene expression data of fibroblasts transduced with LacZ or p63+KLF4.

| PRJNA207551 | ENA

Enrichment of p63, KLF4 and H3K27ac at chromatin in converted and control dermal BJ fibroblasts

Project description:We report changes in enrichment at chromatin of p63, KLF4 and H3K27ac following ectopic expression of wildtype or mutant p63+/- KLF4 for 72 hours in dermal BJ fibroblasts.

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Cross-regulation between Notch and p63 in keratinocyte commitment to differentiation

Project description:Notch signaling promotes commitment of keratinocytes to differentiation and suppresses tumorigenesis. p63, a p53 family member, has been implicated in establishment of the keratinocyte cell fate and/or maintenance of epithelial self-renewal. Here we show that p63 expression is suppressed by Notch1 activation in both mouse and human keratinocytes through a mechanism independent of cell cycle withdrawal and requiring down-modulation of selected interferon-responsive genes, including IRF7 and/or IRF3. In turn, elevated p63 expression counteracts the ability of Notch1 to restrict growth and promote differentiation. p63 functions as a selective modulator of Notch1-dependent transcription and function, with the Hes-1 gene as one of its direct negative targets. Thus, a complex cross-talk between Notch and p63 is involved in the balance between keratinocyte self-renewal and differentiation. Keywords: Notch1, p63, keratinocyte differentiation, gene expression profiling

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p63 controls the enhancer landscape during keratinocyte differentiation

Project description:Here we characterized the transcriptome and epigenome of control keratinocytes during differentiation. Epigenomic analyses showed that the temporal enrichment of p63 motifs in dynamic enhancers underscores the key role of p63 in orchestrating the enhancer landscape during keratinocyte differentiation. The cooperation between p63 and its co-regulating factors, such as RUNX1, is important for the finetuning of gene expression.

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mouse 3T3L1 adipocytes transduced with Lmo3- or LacZ-Adenovirus

Project description:mouse 3T3L1 adipocytes transduced with Lmo3- or LacZ-Adenovirus

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Mutant p63 affects epidermal cell identity through rewiring the enhancer landscape

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>

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Project description:MEK5 is activated by shear stress in large vessel endothelial cells (ECs) and contributes to the suppression of pro-inflammatory changes in the arterial wall. We used microarray analyses of total RNA from MEK5/CA-transduced HDMECs compared to LacZ control-transduced HDMECs to identify distinct classes of several regulated genes, including KLF4, eNOS, and ICAM. We conclude that MEK5 activation by shear stress may modulate inflammatory responses in the microvasculature, and these actions are partly mediated by KLF4.

2010-12-31 | GSE25145 | GEO

MEK5 is Activated by Shear Stress, Activates ERK5 And Induces KLF4 To Modulate TNF Responses in Human Dermal Microvascular Endothelial Cells

2010-12-31 | E-GEOD-25145 | biostudies-arrayexpress

Expression profiling of converted and control dermal BJ fibroblasts

Project description:We report transcriptional changes following ectopic expression of wildtype or mutant p63+/- KLF4 for 72 hours in dermal BJ fibroblasts.

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