Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA281116 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Screening of genes activated by phsiological E2F induced by gorwth stimulation
| PRJNA281704 | ENA
Project description:To identify genes specifically activated by deregulated E2F, we examined gene expression profiles using human normal fibroblasts (HFFs), which were starved of serum and re-stimulated with serum, over-expressed with E2F1 or expressed with adenovirus E1a to forcedly inactivate RB. To identify genes activated by growth stimulation, human normal fibroblasts (HFFs) were starved of serum for 48 hr, infected with control virus, restimulated with serum or left serum-starved for 18 hr and harvested. To identify genes actived by deregulated E2F, HFFs were starved of serum for 48 hr, infected with control virus, adenovirus expressing E2F1 or adenovirus E1a, further cultured in the absence of serum for 18 hr and harvested. Gene expression profiles of ecach sample were examined by DNA microarray.
2015-11-20 | E-GEOD-67887 | biostudies-arrayexpress
Project description:To identify genes specifically activated by deregulated E2F, we examined gene expression profiles using human normal fibroblasts (HFFs), which were starved of serum and re-stimulated with serum, over-expressed with E2F1 or expressed with adenovirus E1a to forcedly inactivate RB.
2015-11-20 | GSE67887 | GEO
Project description:E2F transcription factors control the expression of a large network of cell cycle genes and are essential for S-phase entry. Cancers often demonstrate upregulation of E2F target gene expression, which can be partially explained by loss of the G1/S checkpoint and increased percentages of replicating cells. However, we now demonstrate that cycling individual neoplastic cells can display abnormally high levels of E2F-dependent transcription using single cell RNA sequencing. To test how this affects their DNA damage response, we deleted the atypical E2F transcriptional repressors (E2F7/8) in untransformed cells. This intervention specifically increased the expression of E2F target genes during S and G2-phase without overriding the G1/S-checkpoint. Live cell imaging revealed that cells in S-G2 with deregulated E2F activity failed to arrest and underwent unscheduled mitosis after neocarzinostatin-induced DNA damage. In contrast, cells with physiological E2F-activity completed S-phase and then activated the APC/C-Cdh1 via repression of the E2F-target Emi1, leading to a G1-like arrest. Interestingly, ~30% of these 4N-G1 cells could eventually inactivate APC/CCdh1 to execute a second round of DNA replication and mitosis, resulting in the formation of tetraploid cells. Cells with deregulated E2F activity fail to exit the cell cycle after DNA damage and likely acquire more genetic changes. The observed elevated E2F-dependent transcription in cancer cells could therefore potentially promote malignant progression and reduce sensitivity to anti-cancer drugs.
2020-12-01 | GSE146759 | GEO
Project description:RNA extracted at 240min. Samples are rRNA depleted. Expression measurement of Homo sapiens genes.
2019-07-31 | GSE114179 | GEO
Project description:Transcriptional profiling of Homo sapiens inflammatory skin diseases (whole skin biospies): Psoriasis (Pso), vs Atopic Dermatitis (AD) vs Lichen planus (Li), vs Contact Eczema (KE), vs Healthy control (KO) In recent years, different genes and proteins have been highlighted as potential biomarkers for psoriasis, one of the most common inflammatory skin diseases worldwide. However, most of these markers are not psoriasis-specific but also found in other inflammatory disorders. We performed an unsupervised cluster analysis of gene expression profiles in 150 psoriasis patients and other inflammatory skin diseases (atopic dermatitis, lichen planus, contact eczema, and healthy controls). We identified a cluster of IL-17/TNFα-associated genes specifically expressed in psoriasis, among which IL-36γ was the most outstanding marker. In subsequent immunohistological analyses IL-36γ was confirmed to be expressed in psoriasis lesions only. IL-36γ peripheral blood serum levels were found to be closely associated with disease activity, and they decreased after anti-TNFα-treatment. Furthermore, IL-36γ immunohistochemistry was found to be a helpful marker in the histological differential diagnosis between psoriasis and eczema in diagnostically challenging cases. These features highlight IL-36γ as a valuable biomarker in psoriasis patients, both for diagnostic purposes and measurement of disease activity during the clinical course. Furthermore, IL-36γ might also provide a future drug target, due to its potential amplifier role in TNFα- and IL-17 pathways in psoriatic skin inflammation. In recent years, different genes and proteins have been highlighted as potential biomarkers for psoriasis, one of the most common inflammatory skin diseases worldwide. However, most of these markers are not psoriasis-specific but also found in other inflammatory disorders. We performed an unsupervised cluster analysis of gene expression profiles in 150 psoriasis patients and other inflammatory skin diseases (atopic dermatitis, lichen planus, contact eczema, and healthy controls). We identified a cluster of IL-17/TNFα-associated genes specifically expressed in psoriasis, among which IL-36γ was the most outstanding marker. In subsequent immunohistological analyses IL-36γ was confirmed to be expressed in psoriasis lesions only. IL-36γ peripheral blood serum levels were found to be closely associated with disease activity, and they decreased after anti-TNFα-treatment. Furthermore, IL-36γ immunohistochemistry was found to be a helpful marker in the histological differential diagnosis between psoriasis and eczema in diagnostically challenging cases. These features highlight IL-36γ as a valuable biomarker in psoriasis patients, both for diagnostic purposes and measurement of disease activity during the clinical course. Furthermore, IL-36γ might also provide a future drug target, due to its potential amplifier role in TNFα- and IL-17 pathways in psoriatic skin inflammation.
2014-12-02 | GSE63741 | GEO
Project description: Not available
| S-EPMC2531291 | biostudies-literature
Project description: Not available
| S-EPMC5738339 | biostudies-literature
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
2010-09-25 | GSE24338 | GEO