Ontology highlight
ABSTRACT:
PROVIDER: PRJNA986962 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We used primary mouse microglia to determine whether Bruton's tyrosine kinase (BTK) inhibition could attenuate differential gene expression induced by Fc receptor stimulation.
2024-11-12 | GSE281386 | GEO
Project description:Esophageal cancer-related gene 4 (Ecrg4), a hormone-like peptide, is thought to be a tumor suppressor, however little is known about the mechanism of how Ecrg4 suppresses tumorigenesis. Using the mouse glioma–initiating cell models, we identified Ecrg4 acts as a tumor suppressor in vivo. To characterize the function of Ecrg4 towards microglia, an innate immune cell in central nervous system, we performed gene expression microarray analysis for primary microglia treated with or without recombinant Fc-fused Ecrg4 fragments. We demonstrate here that Ecrg4 fragments, amino acid residues 71-132 and 133-148, which are produced by the proteolitic cleavage, induced the expression of pro-inflammatory cytokines in microglia. Thus, Ecrg4 acts as a cytokine/chemokine inducer, which activates the immune cells to eradicate tumor.
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Project description:We used human induced pluripotent stem cell (iPSC)-derived microglia to determine whether Bruton's tyrosine kinase (BTK) inhibition could attenuate differential gene expression induced by Fc receptor stimulation.
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Project description:Expression data from untreated or Dll4-Fc treated THP1 cell line. We used Dll4-Fc stimulation of AML cells to study whether Notch activation has an impact on AML. We analyzed THP1 cell line in vitro treated with Dll4-Fc or vehicle control to determine genes affected by Notch activation.
2013-01-18 | GSE42259 | GEO
Project description:We used a human induced pluripotent stem cell (iPSC)-derived tri-cultures, comprised of neurons, astrocytes, and microglia, to determine whether Bruton's tyrosine kinase (BTK) inhibition could attenuate differential gene expression induced by Fc receptor stimulation.
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Project description:Systemic inflammation modulates Fc receptor expression on microglia in chronic neurodegeneration
| PRJNA131611 | ENA
Project description:Microglia are the resident macrophages of the central nervous system (CNS). Gene profiling identified the transcriptional regulator Sall1 as a microglia signature gene. Given the high expression of Sall1 in microglia, we sought to identify its function in vivo. The Sall1CreER allele has been targeted into the Sall1 locus, therefore Sall1CreER/fl mice (heterozygous for both alleles) allow inducible ablation of Sall1 expression in microglia after tamoxifen treatment. We performed RNA-seq to examine gene expression profiles of microglia sorted from tamoxifen treated adult Sall1CreER/fl mice and Sall1fl/fl control littermates. Microglia were obtained with > 98% purity and the absence of Sall1 was confirmed in Sall1CreER/fl microglia. We could show that deletion of Sall1 in microglia in vivo resulted in the conversion of these cells from resting tissue macrophages into inflammatory phagocytes leading to altered neurogenesis and disturbed tissue homeostasis. Similar changes in gene expression profiles were found in Sall1-deficient microglia isolated from tamoxifen-treated Cx3cr1CreERSall1fl/fl mice. In these mice, deletion of Sall1 is targeted to CX3CR1+ myeloid cells including microglia and CNS-associated macrophages but not to any other CNS-resident cells. This indicated that Sall1 transcriptional regulation maintains microglia identity and physiological properties in the CNS.
2016-10-19 | E-MTAB-5077 | biostudies-arrayexpress
Project description:Expression data from untreated or Dll4-Fc treated THP1 cell line. We used Dll4-Fc stimulation of AML cells to study whether Notch activation has an impact on AML. We analyzed THP1 cell line in vitro treated with Dll4-Fc or vehicle control to determine genes affected by Notch activation. THP1 cell line was cultured on plate coated with 30 nM Dll4-Fc or vehicle for 48 hours prior to RNA extraction and hybridization to Human Genome U133 Plus 2.0 Affymetrix arrays.
2013-01-18 | E-GEOD-42259 | biostudies-arrayexpress