Effect of p38 SAPK activation on HeLa cells
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PROVIDER: PRJNA483952 | ENA |
REPOSITORIES: ENA
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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:Cell-in-cell(CIC) refers to the active internalization of one or more living cells into another. However, the biological significance and clinical implications of CIC between immune cells and cancer remain unclear. Here, we showed CIC by immunohistochemistry, real-time imaging and multiplex tissue immunofluorescence staining. CD8(+) T cell CIC counts were correlated with lymph node metastasis,T stage, and differentiation in stage I-III CRC. We found CIC counts >4.25 per high-power (magnification 400×) field positively affected metastasis-free survival in stage I-III CRC. Functional experiments demonstrated CD8(+) T CICs increased the migration and invasion in vitro and in vivo. Notably, CD8(+) T CICs were accompanied by greater activation of p38. In addition, blocking p38 using SB203580 significantly suppressed the migration and invasion of CD8(+) T CICs in vitro and in vivo. Moreover, phosphorylated-p38 overexpressing CD8(+) T CICs showed increased expression of cytokeratin 13 (KRT13); however, CD8(+) T CICs pretreated with SB203580 exhibited a significant suppression of KRT13. In summary, Our findings demonstrate that CD8(+) T CIC could be one of the mechanisms of CRC progression. P38 contributes to CD8(+) T “in-cell progression,” and KRT13 may participate in P38- induced “in-cell progression.”
2025-06-01 | GSE270525 | GEO
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:Adult skeletal muscle contains resident Muscle Stem Cells (MuSC) with high myogenic and engraftment potentials, making them suitable for cell therapy and regenerative medicine approaches. However, purification process of MuSC remains a major hurdle to their use in the clinic. Indeed, muscle tissue enzymatic dissociation triggers a massive activation of stress signaling pathways, among which P38 and JNK MAPK, associated with a premature loss of MuSC quiescence. While the role of these pathways in the myogenic progression of MuSC is well established, the extent to which their dissociation-induced activation affects the functionality of these cells remains unexplored. We assessed the effect of P38 and JNK MAPK induction on stemness marker expression and MuSC activation state during isolation by pharmacological approaches. MuSC functionality was evaluated by in vitro assays and in vivo transplantation experiments. We performed a comparative analysis of the transcriptome of human MuSC purified with pharmacological inhibitors of P38 and JNK MAPK (SB202190 and SP600125, respectively) versus available RNAseq resources. We monitored PAX7 protein levels in murine MuSC during muscle dissociation and demonstrated a two-step decline partly dependent on P38 and JNK MAPK activities. We showed that simultaneous inhibition of these pathways throughout the MuSC isolation process preserves the expression of stemness markers and limits their premature activation, leading to improved survival and amplification in vitro as well as increased engraftment in vivo. Through a comparative RNAseq analysis of freshly isolated human MuSC, we provide evidence that our findings in murine MuSC could be relevant to human MuSC. Based on these findings, we implemented a purification strategy, significantly improving the recovery yields of human MuSC. Our study highlights the pharmacological limitation of P38 and JNK MAPK activities as a suitable strategy to qualitatively and quantitatively ameliorate human MuSC purification process, which could be of great interest for cell-based therapies.
2024-06-20 | GSE268475 | GEO
Project description:p38 SAPK and SKIIP induced changes in alternative splicing patterns upon osmostress
| PRJNA482978 | ENA
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