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.
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.
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.
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.
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.
Project description:To eliminate cell-cycle arrested AML cells, we developed a FL-Fc-DM1 drug by conjugating FLT3 liangd Fc fusion protein and mertansine. We used the THP-1 cells as a AML model. The total mRNA of THP-1 cells treated with different concentration of FL-Fc-DM1 were sequenced.
Project description:To eliminate cell-cycle arrested AML cells, we developed a FL-Fc-DM1 drug by conjugating FLT3 liangd Fc fusion protein and mertansine. We used the Molm-13 cells as a AML model. The total mRNA of Molm-13 cells treated with different concentration of FL-Fc-DM1 were sequenced.
Project description:To eliminate cell-cycle arrested AML cells, we developed a FL-Fc-DM1 drug by conjugating FLT3 liangd Fc fusion protein and mertansine. We used the MV-4-11 cells as a AML model. The total mRNA of MV-4-11 cells treated with different concentration of FL-Fc-DM1 were sequenced.
