Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA399882 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5970380.fastq.gz | Fastqsanger.gz | |||
| SRR5970381.fastq.gz | Fastqsanger.gz | |||
| SRR5970382.fastq.gz | Fastqsanger.gz | |||
| SRR5970383.fastq.gz | Fastqsanger.gz | |||
| SRR5970384.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 9 |
Similar Datasets
Project description:Gene expression variation upon folate deficiency and repletion in human foreskin keratinocytes immortalized by HPV16E6E7
2018-12-01 | GSE103044 | GEO
Project description:Upregulation of FOXM1 Induces Genomic Instability in Human Epidermal Keratinocytes
| PRJNA117651 | ENA
Project description:Together with TEAD4 the Hippo pathway effector YAP stimulates chromosomal instability. Verteporfin is known to disrupt the physical YAP/TEAD interaction and tehrefore might prevent from chromosomal instability in liver cancer. Immortalized HCC cell line hepG2 is treated with Verteporfin for 24 hours.
2016-02-11 | E-GEOD-73396 | biostudies-arrayexpress
Project description:Folate deficiency and repletion affects DNA stability and cellular growth of HPV16-immortalized human keratinocytes
| PRJEB25728 | ENA
Project description:The hyper-unstable Chr9p21 locus, harbouring the interferon gene cluster, oncogenes and C9orf72, is linked to multiple diseases. C9orf72 (GGGGCC)n expansions (C9orf72Exp) are associated with incompletely penetrant amyotrophic lateral sclerosis, frontotemporal dementia and autoimmune disorders. C9orf72Exp patients display hyperactive cGAS-STING-linked interferon immune and DNA damage responses, but the source of immuno-stimulatory or damaged DNA is unknown. Here, we show C9orf72Exp in pre-symptomatic and ALS-FTD patient cells and brains cause the folate-sensitive chromosomal fragile site, FRA9A. FRA9A centers on > 33kb of C9orf72 as highly-compacted chromatin embedded in an 8.2Mb fragility zone spanning 9p21, encompassing 46 genes, making FRA9A one of the largest fragile sites. C9orf72Exp cells show chromosomal instability, heightened global- and Chr9p-enriched sister-chromatid exchanges, truncated-Chr9s, acentric-Chr9s and Chr9-containing micronuclei, providing endogenous sources of damaged and immunostimulatory DNA. Cells from one C9orf72Exp patient contained highly-rearranged FRA9A-expressing Chr9 with Chr9-wide dysregulated gene expression. Somatic C9orf72Exp repeat instability and chromosomal fragility are sensitive to folate-deficiency. Age-dependent repeat instability, chromosomal fragility, and chromosomal instability can be transferred to CNS and peripheral tissues of transgenic C9orf72Exp mice, implicating C9orf72Exp as the source. Our results highlight unappreciated effects of C9orf72 expansions that trigger vitamin-sensitive chromosome fragility, adding structural variations to the disease-enriched 9p21 locus, and likely elsewhere.
2024-11-26 | GSE262674 | GEO
Project description:Skin is usually exposed during human exposures to ionizing radiation, however there are few experiments that evaluate the radiation responsiveness of the cells of the epidermis (keratinocytes) and those of the dermis (fibroblasts) in the same studies. We evaluated the transcriptional responses of quiesent primary keratinocytes and fibroblasts from the same individual and compared them with quiescent keratinocytes and fibroblasts that were immortalized by human telomerase (hTert). The primary transcriptional responses to 10-500 cGy ionizing radiation were p53-mediated responses; however, we did identify distinct responses between the keratinocytes and the fibroblasts. Experiment Overall Design: Four cell types (primary keratinocytes, hTert immortalized keratinocytes, primary fibroblasts, hTert immortalized fibroblasts) grown to quiescence, treated with 0, 10, 100 or 500 cGy gamma irradiation, RNA collected at 4 hrs.
2009-06-08 | E-GEOD-14466 | biostudies-arrayexpress
Project description:Previous studies have shown that normal and HPV immortalized keratinocytes are sensitive to TNF anti-proliferative effect. Conversely, HPV18-immortalized keratinocytes are resistant to the cytostatic effect mediated by this cytokine. In this study we have compared gene expression patterns in primary cultures of human foreskin epidermal keratinocytes (PHK or NHFK) and HPV16 (HF698) and HPV18(HF18Nco)-immortalized cell lines, and profile the transcriptional changes 3 and 60 hours after TNF treatment. Keywords: global expression profile, microarray, HPV, TNF
2007-08-25 | GSE4524 | GEO
Project description:Immortalized keratinocytes HaCaT is popular model for skin research (toxicity, irritation, allergic reactions or interaction of cells). They maintain stable keratinocyte phenotype and respond to keratinocyte differentiation stimuli. However, the programs of stratification and expression of differentiation markers in HaCaT keratinocytes are aberrant. HaCaT cells bear two mutant p53 alleles (R282Q and H179Y) which contain Gain-of-Function (GOV) mutations acquired as a result of spontaneous immortalization (mutp53). At the same time, mutp53 acts as a transcription factor, and also affects interaction of p63 protein with its transcription targets. It is known that proteins of the P53 family play an important role in regulating processes of proliferation and differentiation of human keratinocytes.At the same time, the role of mutp53 in these processes is not fully clear. We present data sets obtained as a result of high-performance proteomic analysis of immortalized HaCaT keratinocytes with p53 knockout in two different states: sub-confluent and confluent, which are characterized by different intensity of cell differentiation processes. As a protocol for proteomic profiling of cells, we used the approach of obtaining LC-MS/MS measurements followed by their processing with Progenesis LC-MS software (Nonlinear Dynamics Ltd.)
2022-02-24 | PXD030700 | Pride
Project description:Oxidative stress caused by excessive reactive oxygen species (ROS) disrupts skin and oral epithelial homeostasis and contributes to skin aging, inflammation, periodontitis, and mucosal injury. As the principal defenders in both tissues, keratinocytes may exhibit divergent responses to oxidative stress. However, most existing studies have examined skin or oral keratinocytes in isolation, with few comparative investigations of their tolerance, repair capacity, and antioxidant mechanisms under oxidative stress. In this study, we systematically compared immortalized oral keratinocytes (TIGK) and skin keratinocytes (HaCaT) under hydrogen peroxide (H₂O₂)–induced oxidative stress. Functional analyses, including cell survival, ROS accumulation, wound healing, and proliferation recovery assays, were combined with transcriptomic profiling to evaluate differences in antioxidant and pro-oxidant systems. TIGK exhibited significantly higher survival rates, lower ROS accumulation, and superior migratory and proliferative recovery compared with HaCaT after oxidative insult. Transcriptomic analysis further revealed that TIGK consistently expressed higher levels of antioxidant genes and enzymes. In contrast, HaCaT showed greater ROS accumulation and relatively limited antioxidant defenses. Oral and skin keratinocytes adopt distinct adaptive mechanisms under oxidative stress. The intrinsic redox advantage of oral keratinocytes provides new insights into their rapid wound-healing capacity and may inform strategies to enhance epithelial resilience.
2026-03-12 | GSE308958 | GEO
Project description:Photobiomodulation (PBM) with blue light induces a biphasic dose response curve in proliferation of immortalized human keratinocytes (HaCaT), with a maximum proliferative effect reached with 7.5min (10.35J/cm2). The aim of this study was to test the photobiomodulatory effect of 10.35J/cm2 blue light irradiation on cell proliferation, ROS production and gene expression at different time points after irradiation of HaCaT cells in vitro and to compare the results with the anti-proliferative phase of PBM using blue light with 41.4J/cm2. For 10.35J/cm2 cell proliferation was increased for all measured harvesting time points up to at least 24h after irradiation. ROS concentration was increased 30min after irradiation. However, already 1h after irradiation, cells were able to decrease ROS and stabilize the concentration to the basal level. The sudden increase in ROS was even higher when compared to 41.4J/cm2. However, gene expression analysis did not indicate any sign of apoptosis and even indicated an activation of cell survival mechanisms. Furthermore, comparable to 41.4J/cm2, aryl hydrocarbon receptor (AHR) “battery genes” showed a deregulation after blue light irradiation strengthening the hypothesis of AHR as possible target for blue light irradiation.
2019-10-01 | GSE89085 | GEO