Effect of p38 SAPK activation on HeLa cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA483952 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:HeLa cells were treated with 100 mM NaCl during 2h versus untreated. HeLa cells treated with 100 mM NaCl during 2h versus HeLa cells treated with 100 mM NaCl during 2h after pre-treatment with 10 μM SB203580 for 30 min. Alternative splicing is a crucial mechanism for gene regulation that is modulated in response to a wide range of extracellular stimuli. Stress-activated protein kinases (SAPKs) play a key role in controlling several steps of mRNA biogenesis. Here, we show that osmostress has a major impact on the regulation of alternative splicing (AS), which is partly mediated through the action of the p38 SAPK.
2019-04-16 | GSE117996 | GEO
Project description:Cells have the ability to respond and adapt to environmental changes through the activation of stress-activated protein kinases (SAPKs). Although it has been shown that p38 SAPK signalling participates in the regulation of gene transcription, there is not a comprehensive genome-wide transcription study reported to date describing neither the role of the p38 SAPK on the immediate response to stress and its kinetics nor a comparative vision of the genes that respond to different stimuli that activate the p38 SAPK. Here, we report a whole genome microarray analyses on wild type mouse embryonic fibroblasts (MEFs) treated with different p38 SAPK activators, namely the physiological cytokine TNF alpha, the protein synthesis inhibitor antibiotic anisomycin and osmostress. In addition, we have analysed the contribution of p38 alpha the major isoform of p38 present in MEF cells, in the overall transcription in response to those stimuli by both, the inhibition of p38 SAPK by using a chemical inhibitor (SB203580) and the use of p38 alpha knock out MEFs. Furthermore, we have analysed the kinetics of the gene expression response to osmostress by the p38 SAPK. Two samples have been analysed; wild type Mouse embryonic fibroblast (WT-MEFs) and MAPK p38alfa knock out MEFs (KO-MEFs) respectively treated with 11 and 4 different treatments. Each experiment was performed in duplicate and referenced to a pool of two non-treated WT MEFs.
2010-09-29 | E-GEOD-18320 | biostudies-arrayexpress
Project description:Cells have the ability to respond and adapt to environmental changes through the activation of stress-activated protein kinases (SAPKs). Although it has been shown that p38 SAPK signalling participates in the regulation of gene transcription, there is not a comprehensive genome-wide transcription study reported to date describing neither the role of the p38 SAPK on the immediate response to stress and its kinetics nor a comparative vision of the genes that respond to different stimuli that activate the p38 SAPK. Here, we report a whole genome microarray analyses on wild type mouse embryonic fibroblasts (MEFs) treated with different p38 SAPK activators, namely the physiological cytokine TNF alpha, the protein synthesis inhibitor antibiotic anisomycin and osmostress. In addition, we have analysed the contribution of p38 alpha the major isoform of p38 present in MEF cells, in the overall transcription in response to those stimuli by both, the inhibition of p38 SAPK by using a chemical inhibitor (SB203580) and the use of p38 alpha knock out MEFs. Furthermore, we have analysed the kinetics of the gene expression response to osmostress by the p38 SAPK.
2010-09-29 | GSE18320 | GEO
Project description:Alternative splicing is a crucial mechanism for gene regulation that is modulated in response to a wide range of extracellular stimuli. Stress-activated protein kinases (SAPKs) play a key role in controlling several steps of mRNA biogenesis. Here, we show that osmostress has a major impact on the regulation of alternative splicing (AS), which is partly mediated through the action of the p38 SAPK. Remarkably, a splicing network analysis revealed a functional connection between p38 and the spliceosome component SKIIP. Depletion of SKIIP abolished a significant part of the p38-mediated alternative splicing.
2019-04-16 | GSE117699 | GEO
Project description:JBIR-140 (prethioviridamide) effect on HeLa S3 cells
| PRJNA509785 | ENA
Project description:Background: Magnesium transporter subtype 1 (MAGT1) is involved in animal development and cell differentiation. Thus far, researches on MAGT1 are mainly focused on Cardiomyocyte regulation and differentiation, but rare research has been reported on cell proliferation, especially concerning the underlying molecular mechanisms. Methods: HeLa cells were transiently knock down with different SiRNAs and processed for RNA sequencing and bioinformatics analysis, western blot, real-time PCR as well as cell cycle assays. Results: We showed that cell proliferation was significantly restricted with S-phase arrest in MAGT1 knock down cells, which was further confirmed by the up expression of p21, CCNA1 and CCNB1, while down expression of CCND1, CCNE1 and CDK4. Knocking down MAGT1 also resulted in significant transcriptional expression changes of 1599 target genes analyzed by RNA sequencing. The bioinformatics analysis showed that MAGT1 was related to MAPK signaling pathway. Western blot analysis confirmed that the phosphorylation of ERK1/2 and p38 exhibited a remarkable reduction in MAGT1 downregulated group. Conclusion: MAGT1 is critical in HeLa cell proliferation, S-phase progress and ERK/p38 MAPK signaling pathway, indicating that MAGT1 might be a novel target of anticancer research.
2022-02-02 | GSE166084 | GEO
Project description:Analysis of HeLa cells treated with histone deacetylase inhibitor SAHA for 24hr. Results provide insight into the effect of SAHA on the activation of lysosomal and autophagy pathways
2019-07-08 | GSE106175 | GEO
Project description:Differentiation therapy with all-trans retinoic acid (ATRA) is well established for acute promyelocytic leukemia (APL). However, the narrow application and tolerance development of ATRA remain to be improved. A number of kinase inhibitors have been reported to induce differentiation. In this study, we challenged several combinations of these kinase inhibitors. As a result, we found that the combination of Akt inhibitor Triciribine (TCN) and several p38 MAPK inhibitors have profound effect for differentiation in several myeloid cell lines. To reveal the molecular mechanisms involved in TCN and p38 MAPK inhibitor induced differentiation, we performed microarray analysis.
2023-06-27 | GSE235632 | GEO
Project description:p38 SAPK and SKIIP induced changes in alternative splicing patterns upon osmostress
| PRJNA482978 | ENA
Project description:HAMLET triggers a p38- and ER stress-dependent death response in carcinoma cells. Transcriptome and proteome analysis detected an increase in p38 expression and phosphorylation exclusively in carcinoma cells and p38 inhibitors delayed the death response to HAMLET in carcinoma and lymphoma cells. ER stress gene expression was also increased in tumor cells and HAMLET triggered rapid XBP1 mRNA splicing, eIF2a phosphorylation, and ATF6 cleavage as well as Hsc70 and CHOP activation, suggesting that ER stress caused by HAMLET may trigger p38 phosphorylation and death. The p38 inhibitor reduced the transcription of both p38 and ER stress gene transcription. Healthy differentiated cells, in contrast, showed no alteration in p38 signaling but a rapid innate immune response was detected and the cells survived HAMLET challenge. 2 cell lines, time course, HAMLET treatment
2010-08-24 | E-GEOD-23772 | biostudies-arrayexpress