Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7796664_1.fastq.gz | Fastqsanger.gz | |||
| SRR7796664_2.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:This study shows that croton oil has a specific inflammatory signature involving altered expression of cytokines that is quantitatively altered by long-term LC ablation.
2021-03-23 | GSE143569 | GEO
Project description:The expression of lysozyme was significantly up-regulated in macrophages treated with butyrate. In order to prove the relationship between Lysine Crotonylation modification and lysozyme up-regulation, lysine sites occured croton modification were detected and analyzed.
2025-06-16 | PXD029698 | Pride
Project description:Croton tiglium Transcriptomes from 5 different tissues
| PRJNA416498 | ENA
Project description:Strong inhibition of NF-kB signaling in the epidermis results in spontaneous skin inflammation in mice and men. Since there is evidence for linkage between polymorphisms within the NF-kB signaling pathway and human inflammatory skin phenotypes, we asked whether partial functional inhibition of NF-kB signaling in epidermal keratinocytes can modulate clinically relevant skin inflammation. We therefore mutated rela specifically in the epidermis of mice (RelAE-MUT mice). These mice show no inflammatory phenotype. Induction of contact allergy, but not croton oil induced irritant dermatitis, resulted in stronger ear swelling and increased epidermal thickness in RelAE-MUT mice. Both contact allergen and croton oil treatment led to increase expression of calgranulins A and B (S100A8/ A9) in RelAE-MUT mice. Epidermal hyperproliferation in RelAE-MUT mice was non-cell autonomous since cultured primary epidermal keratinocytes from RelAE-MUT mice showed reduced proliferation compared to controls. These results demonstrate that epidermal RelA specifically regulates DTH-induced skin inflammation. In addition, we here describe an essential but non- specific function of RelA in the protection of epidermal keratinocytes from apoptosis. Our study identifies new functions of NF-kB signaling in the epidermis and corroborates a specific role of epidermal keratinocytes in the regulation of skin inflammation
2014-12-01 | GSE56067 | GEO
Project description:Even though cutaneous atrophy is the major adverse effect of topical glucocorticoids, its molecular mechanisms are poorly understood. We found that glucocorticoids strongly increased the expression of REDD1 (regulated in development and DNA damage response 1), a stress-inducible inhibitor of mTOR, in mouse and human epidermis. We found that REDD1 knockout animals are partially resistant to glucocorticoid-induced epidermal and subcutaneous adipose atrophy which correlated with the protection of CD34+ follicular epithelial stem cells as well as p63+ keratinocyte progenitors in REDD1 knockout epidermis during chronic steroid treatment. At the same time, REDD1 knockout did not affect anti- inflammatory effect of glucocorticoids, as evaluated by ear edema test. Expression profiling revealed that ~ 50% of the glucocorticoid receptor (GR) target genes were not activated in epidermis of REDD1 knockouts, however, the negative effect of glucocorticoids on gene expression was similar to that in w.t. animals. Overall, our findings reveal a novel pathway in GR activation by its target gene/protein REDD1; and indicate an important role of REDD1 in glucocorticoid-induced skin atrophy, and maintenance of the epidermis and subcutaneous adipose. In addition, our findings form the foundation for the development of safer topical glucocorticoid treatment regimens by combining this therapy with REDD1 inhibitors. Seven wk old B6D2 females in the telogen stage of the hair cycle were shaved, and treated 3 days later. Glucocorticoid FA was applied topically (2 ug/animal) in 200 ul acetone to the back skin once or up to four applications every third day as described previously (Chebotaev et al., 2007b). Control animals were treated with acetone only. Skin was harvested 24 h after last FA application or 4-8 h after single FA application as indicated in Figure legends. To evaluate the anti-inflammatory effect of glucocorticoid FA in REDD1 KO and w.t. B6x129 mice, we used ear edema test (Schoepe et al., 2010; Schäcke et al., 2004; Park et al., 2006). Seven wk old female animals were pretreated with FA or vehicle applied to the back of the ear lobe one h before application of nonspecific contact irritant croton oil . Mice were sacrificed and ears were harvested nine hours after CO application, the time point at which we observed maximum ear edema in F1 C57Bl x 129 animals (data not shown). Four mm ear punch biopsies were immediately weighted to assess ear edema. Animals were injected i.p. with bromodeoxyuridine 1 hr before skin was harvested. Total RNA from murine epidermis and whole human skin was isolated with RiboPure kit (Ambion). Total RNA from murine s.c. adipose was isolated with RNeasy Lipid Tissue Kit (Qiagen). The RNA samples were treated with TURBOTM DNase (Ambion). Purity of RNA samples isolated from epidermis and s.c. fat was confirmed by the expression of adipose and keratinocyte cell markers.
2014-08-01 | E-GEOD-59151 | biostudies-arrayexpress
Project description:This study aims to investigate the DNA methylation patterns at transcription factor binding regions and their evolutionary conservation with respect to binding activity divergence. We combined newly generated bisulfite-sequencing experiments in livers of five mammals (human, macaque, mouse, rat and dog) and matched publicly available ChIP-sequencing data for five transcription factors (CEBPA, HNF4a, CTCF, ONECUT1 and FOXA1). To study the chromatin contexts of TF binding subjected to distinct evolutionary pressures, we integrated publicly available active promoter, active enhancer and primed enhancer calls determined by profiling genome wide patterns of H3K27ac, H3K4me3 and H3K4me1.
2022-10-20 | E-MTAB-11946 | biostudies-arrayexpress