Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA167617 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We have examined the changes in gene expression aftert reatment of A549 cells, a cultured alveolar epithelial cells, with flagellin and transforming growth factor beta 1. In this dataset, we include the expression data obtained from A549 cells after treatment with purified flagellin or transforming growth factor beta 1 receptor. The analysis indicated that flagellin induced a change in gene expression that was similar to the changes induced by transforming growth factor 1.
2012-10-31 | GSE38309 | GEO
Project description:We have examined the changes in gene expression aftert reatment of A549 cells, a cultured alveolar epithelial cells, with flagellin and transforming growth factor beta 1. In this dataset, we include the expression data obtained from A549 cells after treatment with purified flagellin or transforming growth factor beta 1 receptor. The analysis indicated that flagellin induced a change in gene expression that was similar to the changes induced by transforming growth factor 1. A549 cells were treated with flagellin or transforming growth factor 1 for 24 h. Total RNA was extracted and reverse transcribed to cDNA. Synthesized cDNA was fragmented and labeled with biotin. The biotinylated cDNA was hybridized to to an Affymetrix GeneChip Array, and probe signal intensities were captured.
2012-10-31 | E-GEOD-38309 | biostudies-arrayexpress
Project description:T Cell Receptor Based Therapy of Metastatic Colorectal Cancer With mRNA-engineered T Cells Targeting Transforming Growth Factor Beta Receptor Type II (TGFβII)
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Project description:RATIONALE: Measuring levels of transforming growth factor-beta (TGF-beta) in the blood of patients with epithelial cancers (head and neck, lung, breast, colorectal, and prostate) may help doctors predict how patients will respond to treatment with radiation therapy.
PURPOSE: This research study is measuring levels of TGF-beta in patients with epithelial cancers who are undergoing radiation therapy.
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Project description:Human intestinal macrophages contribute to tissue homeostasis in noninflamed mucosa through profound down-regulation of pro-inflammatory cytokine release. Here, we show that this down-regulation extends to Toll-like receptor (TLR)-induced cytokine release, as intestinal macrophages expressed TLR3-TLR9 but did not release cytokines in response to TLR-specific ligands. Likely contributing to this unique functional profile, intestinal macrophages expressed markedly down-regulated adapter proteins MyD88 and Toll interleukin receptor 1 domain-containing adapter-inducing interferon beta, which together mediate all TLR MyD88-dependent and -independent NF-kappaB signaling, did not phosphorylate NF-kappaB p65 or Smad-induced IkappaBalpha, and did not translocate NF-kappaB into the nucleus. Importantly, transforming growth factor-beta released from intestinal extracellular matrix (stroma) induced identical down-regulation in the NF-kappaB signaling and function of blood monocytes, the exclusive source of intestinal macrophages. Our findings implicate stromal transforming growth factor-beta-induced dysregulation of NF-kappaB proteins and Smad signaling in the differentiation of pro-inflammatory blood monocytes into noninflammatory intestinal macrophages. Comparison of unstimulated monocytes and macrophages, and flagellin stimulated monocytes and macrophages.
2010-07-07 | E-GEOD-22373 | biostudies-arrayexpress
Project description:Transforming growth factor-beta (TGF-beta) transmits signals that facilitate cancer progression. Especially, epithelial-mesenchymal transition (EMT) induced by TGF-beta is considered to crucially contribute to the malignant phenotype of cancer cells. Here we report that the EMT-associated cellular responses induced by TGF-beta are mediated through distinct signaling pathways that diverge at Smad3; cell motility and epithelial marker downregulation are Smad3-dependent while mesenchymal marker induction is not. Furthermore, using a chimeric protein approach in SMAD3 knockout A549 cells, we found that the beta 4 region in the MH1 domain of Smad3 is indispensable for TGF-beta–induced cell motility, but not for epithelial marker downregulation. A transcriptome analysis was performed using A549 cells expressing Smad3 mutant of the MH1 domain.
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Project description:The aim of the study was to characterize the transcriptional profiles of two cholangiocarcinoma cell lines (HuCCT1 and Huh28) after a treatment with Transforming Growth Factor beta (TGF-beta).
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