Project description:Connectivity map analysis using an AML-specific cMYB gene signature (Walf-Vorderwulbecke et al. Leukemia. 2018;32(4):882-889. 10.1038/leu.2017.317) identified withaferin A (WFA) as a candidate cMYB deregulating agent in AML. In order to validate the predicted effect of WFA on cMYB function, RNAseq analysis was performed on THP1 cells following exposure to DMSO or 1mM WFA for 6 hours.
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.
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 an inducible shRNA system and RNA-Seq to examine gene expression changes in acute myeloid leukemia THP1 cells following silencing of RUVBL2. RUVBL2 is a AAA+ ATPase that functions in a number of cellular processes, including chromatin remodeling and transcriptional control, and is critical for survival of acute myeloid leukemia cells and in vivo disease progression.
Project description:We report the use of complementary peptide antigen enrichment and comprehensive mass spectrometric acquisition strategies to provide in-depth immunopeptidome data for AML cell line THP1
Project description:We used an inducible shRNA system and RNA-Seq to examine gene expression changes in acute myeloid leukemia THP1 cells following silencing of RUVBL2. RUVBL2 is a AAA+ ATPase that functions in a number of cellular processes, including chromatin remodeling and trnascriptional control, and is critical for survival of acute myeloid leukemia cells and in vivo disease progression.
Project description:To experimentally investigate the function of hsa-miR-511-5p in AML monoblasts, we employed miRNA mimic mediated up-regulation of miR-511 in THP1 cells and subsequently analyzed a comprehensive gene expression profile. 4 samples of two independent miRNA mimic experiments were analyzed. THP1 monoblasts were transfected with 30 nM of Ambion Pre-miR miRNA Precursors (hsa-miR-511-5p AM10237 or negative Control #1 AM17110, Life Technologies).