Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19910549_1.fastq.gz | Fastqsanger.gz | |||
| SRR19910549_2.fastq.gz | Fastqsanger.gz | |||
| SRR19910550_1.fastq.gz | Fastqsanger.gz | |||
| SRR19910550_2.fastq.gz | Fastqsanger.gz | |||
| SRR19910551_1.fastq.gz | Fastqsanger.gz |
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Project description:The genetic expression profile of a Wnt signal agonist, BIO, was evaluated in human primary keratinocytes. Accelerating scaling up of primary keratinocytes benefits skin autografts for severely burned patients. Wnt signal, a conserved pathway controlling cell cycle and morphogenesis of embryo, has been postulated to promote the cell proliferation and tumorigenesis in adult. Here, the effects of Wnt signal on the growth of interfollicular keratinocytes were investigated. We demonstrated that recombinant Wnt3a significantly promoted the primary keratinocyte growth at a low cell density. A well-characterized GSK-3beta inhibitor, BIO, activated the Wnt signals and also enhanced the colony formation of keratinocytes dose-dependently. Gene expression profile of the BIO-treated keratinocytes revealed the linkage of the BIO with the cell mitosis and indicated that epithelial cell adhesion molecule (EpCAM), a Wnt target gene, was upregulated. Comparing to the EpCAM- keratinocytes, the EpCAM+ cells showed higher proliferation rate and efficacy of the colony formation. Especially, inhibiting the EpCAM expression by shRNA attenuated the proliferation effect of BIO and the growth advantage of the EpCAM+ keratinocytes. These evidences emphasize the positive role of canonical Wnt and EpCAM on the regulation of cell growth and self-renewal for human keratinocytes.
2012-10-01 | E-GEOD-40233 | biostudies-arrayexpress
Project description:Extracellular vesicles (EVs) are membrane vesicles released by all cell types and contain proteins and non-coding RNAs, which are transported into recipient cells to regulate their signal transduction and functions. Increasing evidence has demonstrated that EV shuttling is an effective means of bio-molecule transportation among various cell types in the tumor microenvironment, and thus plays a critical role in regulating cancer cell biology. Previous studies have shown that TAMs are an important source of extracellular vesicles and the extracellular vesicles released by TAMs can promote the invasiveness of breast cancer cells. In this study, we studied the differential expression of TAM EV and the donor cells.
2019-01-22 | GSE123473 | GEO
Project description:In response to infection, antigen-specific CD8+ T cells are primed in the T cell zone of secondary lymphoid organs and differentiate into cytotoxic effector T (TC) cells. Concurrently, CD4+ T cells differentiate into follicular helper T (TFH) cells that localize to B cell follicles and promote protective antibody responses. During unresolved infections, however, some viruses including human immunodeficiency virus (HIV) or Epsteinâ??Barr virus (EBV) escape immune control and persist in TFH cells and B cells, respectively. Exclusion of Tc cells from B cell follicles is thought to be a major mechanism of immune evasion. New strategies are therefore needed to eradicate infected cells in follicles for a permanent cure. Using mouse infection models and human samples, we here identify a specialized group of TC cells expressing the chemokine receptor CXCR5 that can selectively enter B cell follicles and eradicate infected TFH and B cells. We demonstrate that differentiation of these cells, which we term follicular cytotoxic T (TFC) cells, requires the transcription factors Bcl6, E2A and Tcf1, whereas the transcriptional regulators Blimp1, Id3 and Id2 inhibit their development. We demonstrate that Blimp1 and E2A directly regulate Cxcr5 expression, and together with Bcl6 and Tcf1 form a transcriptional circuit that guides the TFC differentiation. The identification of a follicular subset of TC cells has far reaching implications for developing better strategies for the control of infections that target B cells and TFH cells and for the eradication of B cell derived malignancies. There is no associated input. The E2A Bio-ChIP-seq was performed with total thymocytes from Tcf3Bio/Bio Rosa26BirA/BirA mice
2016-08-01 | E-GEOD-84974 | biostudies-arrayexpress
Project description:This study investigated early host reactions to implanted materials to predict successful tissue regeneration with implant. Three kinds of scaffold, i.e., non-coat, collagen-coated, and PMB-coated porous polystylene scaffolds were implanted subcutaneously in mice dorsal area. Those scaffolds were used as bio-incomopatible materials, appropriate materials for tissue regeneration (bio active), and inappropriate to regenration (bio-inert) scaffolds. Seven days after implantation, scaffolds were explanted and total RNA was isolated from infiltrated host cells into scaffold by laser microdissection. Gene expressions of cells in collagen- and PMB-coated scaffold were normalized using results of non coat scaffold. Genes with more than 2-fold difference between collagen and PMB were picked up and narrowed to related keywords; inflammation, angiogenesis, wound healing, and mcrophage polarization. Among those genes, interluekin (IL)-1beta which promote both inflammation and wound healing was up-regulated in collagen-coated scaffold. On the other hand, IL-10 which suppress both inflammation and wound healing was up-regulated in PMB-coated scaffold. Angiogenesis-promoting genes were up-regulated and angiogenesis suppressve genes were suppressed in collagen. Up-regulation of IL-1b and the angiogenesis-relating genes inside the porous scaffolds are the possibly important factors for controlling tissue regeneration.
2014-01-23 | GSE52053 | GEO
Project description:Development of radiation medical countermeasures under the U.S. Food and Drug Administration Animal Rule requires the capability to translate an effective animal to human drug dose. One method of human dose translation is using a biomarker and determining drug doses that modulate the biomarker to the desired level. BIO 300 Oral Powder (BIO 300) is a prophylactic radiation medical countermeasure that is currently being developed following the Animal Rule. The present study aimed to identify biomarkers that can be used for human dose conversion by conducting transcriptomics of whole blood collected from BIO 300-treated CD2F1 mice in the presence and absence of total-body irradiation (TBI). Mice were treated with vehicle or 50, 100 or 200 mg/kg BIO 300, twice daily, for 6 days. Whole blood samples were collected 24 and 48 h after the last dose of the drug. Animals were also treated with vehicle or 200 mg/kg BIO 300 for 6 days prior to 9.2 Gy TBI 24 h after the last dose, with blood collection 24 h after irradiation. RNA sequencing demonstrated 100 – 200 mg/kg doses caused significantly more differential gene expression at 48 h post-drug dose compared to 50 mg/kg. Pathway analysis of the transcriptome profile from vehicle-treated/radiation-exposed mice revealed that many inflammatory signaling pathways were activated in these animals. Signaling pathways enriched in BIO 300-treated/TBI mice were involved in cellular stress and immune response and were predicted to be inhibited. We also identified pathways that were in inverse states (activation/inhibition) in vehicle and BIO 300-treated mice with TBI. There were two pathways specifically activated in vehicle-treated animals with TBI and inhibited in BIO 300-treated animals (with or without TBI), pathogen-induced cytokine storm signaling and S100 family signaling. In comparison to previously published human data, pulmonary fibrosis idiopathic signaling and wound healing signaling were enriched in healthy volunteers treated with BIO 300 and BIO 300-treated mice with TBI. In all, four signaling pathways were identified that were activated in vehicle-treated animals exposed to total body radiation but inhibited in irradiated animals or healthy humans treated with BIO 300. These pathways should be explored to identify potential biomarkers of BIO 300 that can be used for human dose translation.
2024-08-14 | GSE268247 | GEO
Project description:This study investigated early host reactions to implanted materials to predict successful tissue regeneration with implant. Three kinds of scaffold, i.e., non-coat, collagen-coated, and PMB-coated porous polystylene scaffolds were implanted subcutaneously in mice dorsal area. Those scaffolds were used as bio-incomopatible materials, appropriate materials for tissue regeneration (bio active), and inappropriate to regenration (bio-inert) scaffolds. Seven days after implantation, scaffolds were explanted and total RNA was isolated from infiltrated host cells into scaffold by laser microdissection. Gene expressions of cells in collagen- and PMB-coated scaffold were normalized using results of non coat scaffold. Genes with more than 2-fold difference between collagen and PMB were picked up and narrowed to related keywords; inflammation, angiogenesis, wound healing, and mcrophage polarization. Among those genes, interluekin (IL)-1beta which promote both inflammation and wound healing was up-regulated in collagen-coated scaffold. On the other hand, IL-10 which suppress both inflammation and wound healing was up-regulated in PMB-coated scaffold. Angiogenesis-promoting genes were up-regulated and angiogenesis suppressve genes were suppressed in collagen. Up-regulation of IL-1b and the angiogenesis-relating genes inside the porous scaffolds are the possibly important factors for controlling tissue regeneration. Three-condition experiment, host cells infiltrated in non coat (reference), collagen-coated, and PMB-coated scaffolds. Two-microarray condition experiments, collagen vs. non coat and PMB coat vs. non coat. Hybridization: 2 replicates. Scanning: 3 replicates. Biological experiments: once.
2014-01-23 | E-GEOD-52053 | biostudies-arrayexpress
Project description:Carboxy-terminally tagged MOZ (Flag-V5-BIO tagged) was detected by ChIP-seq using anti-V5 antibody (Sigma, A7345) to precipitate chromatin associated with MOZ
2019-07-23 | GSE134607 | GEO