E-MTAB-3474
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-3474 | ExpressionAtlas | 2015-04-08
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:Skeletal myocyte differentiation involves fusion of myoblasts to multinucleated myotubes. In vitro differentiation can be induced by serum withdrawal. The differentiation process is negatively regulated by pathological concentrations of TNF-alpha but can be positively regulated by IGF1. This study focuses on elucidating the expression kinetics of mRNAs right after induction of differentiation (4 hours), during very early differentiation (12 h), early differentiation (24 h) as well as later differentiation (72 h) and how gene expression is modulated by TNF-alpha or IGF1, respectively.
2015-04-05 | E-MTAB-3474 | biostudies-arrayexpress
Project description:Primary human skeletal muscle cells (hSkMCs) were cultured in growth medium and a fraction of dishes was switched to differentiation medium and to differentiation medium containing 2 x 103 U/ml human recombinant TNF-alpha (Roche Applied Science, Basel, Switzerland), respectively. hSkMCs cells were harvested 24 h (myoblasts day one and myotubes day one without and with 2 x 103 U/ml TNF-alpha, respectively,) after the induction of differentiation. The experiments were performed in triplicates.
2010-07-07 | E-MTAB-299 | biostudies-arrayexpress
Project description:In our previous study, we found that TNF-alpha (100ng/mL) different treatment times have opposing effects on BMSC osteogenesis. To investigate the roles of TNF-alpha in the osteogenic differentiation of hBMSCs, we performed gene microarray to detected the gene expression of hBMSCs with or without TNF-alpha during osteogenesis on days 3 and 4.
2021-06-04 | GSE176086 | GEO
Project description:To investigate the TNF-α in the regulation of L929 cells.We performed gene expression profiling analysis using data obtained from RNA-seq of L929 cells activated by TNF-α.
2022-05-09 | GSE202376 | GEO
Project description:The increased secretion of pro-inflammatory cytokines, such as tumor necrosis factor-alpha, is often associated with adipose tissue dysregulation, which often accompanies obesity. High levels of TNF-alpha have been linked to development of insulin resistance in several tissues and organs, including skeletal muscle and the liver. In this study, we examined the complex regulatory roles of TNF-alpha in murine hepatocytes utilizing a combination of global proteomics and phosphoproteomics analyses. Our results show that TNF-alpha promotes extensive, dynamic changes not only of protein levels, but also the dynamics of their downstream phosphorylation signaling states. We provide evidence that TNF-alpha likely induces DNA replication, and promotes G1/S transition through the activation of the MAPK pathway. Our data also highlights several other novel proteins, many of which are regulated by phosphorylation and that play a role in the progression and development of insulin resistance in hepatocytes.
2021-04-20 | MSV000087248 | MassIVE
Project description:Mesenchymal stem cells (MSCs) can differentiate into endothelial cells; however, the mechanisms underlying this process in the tumor microenvironment (TME) remain elusive. This study shows that tumor necrosis factor alpha (TNF-α), a key cytokine present in the TME, promotes the endothelial differentiation of MSCs by inducing vascular endothelial growth factor receptor 2 (VEGFR2) gene expression. EGR1 is a member of the zinc-finger transcription factor family induced by TNF-α. Our findings indicate that EGR1 directly binds to the VEGFR2 promoter and transactivates VEGFR2 expression. We also demonstrate that EGR1 forms a complex with c-JUN activated by c-JUN N-terminal kinase (JNK) to promote VEGFR2 transcription and endothelial differentiation in MSCs in response to TNF-α stimulation. The shRNA-mediated silencing of EGR1 or c-JUN abrogates TNF-α-induced VEGFR2 transcription and the endothelial differentiation of MSCs. Collectively, these findings demonstrate that the JNK-EGR1 signaling axis plays a crucial role in the TNF-α-induced endothelial differentiation of MSCs in the TME, which could be a potential therapeutic target for solid tumors vasculatures.
2022-10-06 | GSE214834 | GEO
Project description:MCF-7 cells were stimulated with TNF-alpha in order to identify IKKb substrates. conditions: TNF alpha stimulation TNF alpha stimulation + SC-514 IKK (kinase dead mutant) + TNF alpha stimulation IKK(WT) + TNF alpha stimulation basal Already validated IKK substrates were used to train random forest and to predict new substrates. Among other interesting candidates we validated AEG-1 (S298) as an IKKb substrate. We provide evidence that IKKb-mediated AEG-1 phosphorylation is essential for IkBa degradation as well as NF-kB-dependent gene expression and cell proliferation, which correlate with cancer patient survival in vivo. (replicate 1 out of at least 2)
2018-10-17 | PXD001873 | Pride
Project description:Tumour necrosis factor-alpha (TNF-α), one of the pro-inflammatory cytokines mediating the local inflammatory process in joints, has an inhibitory effect on cartilage formation and has a detrimental effect on stem cell-based cartilage regeneration for the treatment of osteoarthritis (OA). However, the mechanisms behind this inhibitory effect are still poorly understood. Mitochondria are important organelles that play a vital role in maintaining the structure and function of the cell. Our study aimed to investigate the role and mechanisms of regulation of mitochondrial fusion and fission in the chondrogenic differentiation of human adipose stem cells (hADSCs) in the absence and presence of TNF-α. Affmetrix PrimeViewTM chips for gene expression profiling.
2023-05-01 | GSE221879 | GEO
Project description:Schistosoma mansoni is the major causative agent of schistosomiasis in the Americas. This parasite takes advantage from host signaling molecules such as cytokines and hormones to complete its development inside the host. TNF-α is the most important cytokine involved in the inflammatory response when cercaria, the infective stage, penetrates the human skin and a severe inflammatory response is started. In this work the authors describe the complete sequence of a possible TNF-α receptor in S. mansoni and detect that the receptor is most highly expressed in cercaria among all life cycle stages. In an attempt to mimic the situation at the site of skin penetration cercariae have been mechanically transformed in vitro into schistosomula and immediately exposed to human TNF-α . Exposure of these early schistosomula to the human hormone caused a large-scale change in the expression of parasite genes. Exposure of adult worms to human TNF-α caused gene expression changes as well, although the set of parasite altered genes was entirely different from that of schistosomula. This work increases the number of known signaling pathways of the parasite, and opens new perspectives into understanding the molecular components of TNF-α response as well as possibly interfering with parasite-host interaction.
2009-12-15 | GSE16261 | GEO
Project description:Schistosoma mansoni is the major causative agent of schistosomiasis in the Americas. This parasite takes advantage from host signaling molecules such as cytokines and hormones to complete its development inside the host. TNF-α is the most important cytokine involved in the inflammatory response when cercaria, the infective stage, penetrates the human skin and a severe inflammatory response is started. In this work the authors describe the complete sequence of a possible TNF-α receptor in S. mansoni and detect that the receptor is most highly expressed in cercaria among all life cycle stages. In an attempt to mimic the situation at the site of skin penetration cercariae have been mechanically transformed in vitro into schistosomula and immediately exposed to human TNF-α . Exposure of these early schistosomula to the human hormone caused a large-scale change in the expression of parasite genes. Exposure of adult worms to human TNF-α caused gene expression changes as well, although the set of parasite altered genes was entirely different from that of schistosomula. This work increases the number of known signaling pathways of the parasite, and opens new perspectives into understanding the molecular components of TNF-α response as well as possibly interfering with parasite-host interaction.
2009-12-15 | GSE16260 | GEO