Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA323419 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Gene expression signature of the T-ALL cell line LOUCY treated with 1µM (+)-JQ1 for 48h
| PRJNA323424 | ENA
Project description:We analyzed the transcriptional consequences of the BET bromodomain inhibitor JQ1 in the T-ALL cell line LOUCY by microarray analysis. Short-term exposure to a low dose of JQ1 (4h, 250nM) provided insights in the genes whose expression was immediately affected by BET bromodomain inhibition. Significantly downregulated genes upon short-term drug treatment included stem-cell associated genes and putative oncogenes such as BAALC, WT1, MN1, MEF2C, LMO1 and LMO2. Genes associated with the 500 highest ranked enhancer regions in LOUCY, were significantly enriched in genes downregulated after JQ1 treatment.
2016-12-15 | GSE81915 | GEO
Project description:Low-pass sequencing of Trueprime amplified LOUCY cell line DNA
| PRJNA318625 | ENA
Project description:Bromodomain and extra terminal domain (BET) inhibition reduces occupancy of BET-family proteins at promoter and enhancer sites resulting in changes in the transcription of specific genes. We used microarray profiling to investigate the transcriptional changes induced by BET inhibitor JQ1 treatment in DV90 cells to identify the underlying changes of gene regulation that lead to JQ1 sensitivity. DV90 cells (JQ1 sensitive non-small cell lung cancer cell line) were treated with 135 nM (IC50) or 785 nM (IC90) of JQ1 for 4h and 24h. DMSO treated controls served as reference and at least four replicates per condition were collected. RNA was extracted and hybridized to Affymetrix HuGene-2.1ST microarrays to identify treatment induced transcriptional changes.
2016-03-31 | E-GEOD-75960 | biostudies-arrayexpress
Project description:RNA sequencing was performed on biological triplicates of LOUCY and PEER cells treated with 100nM GSK2879552 for 48h versus their corresponding DMSO treatment controls. GSK2879552 is a potent, selective and orally bioavailable inhibitor of the lysine-specific histone demethylase 1 (LSD1). Gene expression was severely affected by LSD1 inhibition. Pathway analysis performed on the differentially expressed genes following 48hrs of LSD1i treatment clearly showed an increased apoptotic gene signature (CASP3, CASP8) and enhanced expression of genes associated with TRAIL signaling. Furthermore, pre-ranked Gene Set Enrichment Analysis (GSEA) revealed that genes upregulated after LSD1 inhibition in LOUCY showed significant enrichment for transcripts that are down in hematopoietic stem cells and early T lymphocytes. In contrast, important components of the Notch, WNT and SMAD signalling complex were significantly down regulated upon short-term LSD1i treatment in LOUCY cells. In line with this notion, pre-ranked GSEA also revealed that LSD1i resulted in decreased expression of genes that significantly overlap with an oncogenic MYC signature.
2017-02-03 | GSE83126 | GEO
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
2010-09-25 | GSE24338 | GEO
Project description:We analyzed the transcriptional consequences of the BET bromodomain inhibitor JQ1 in the T-ALL cell line LOUCY by microarray analysis. Sustained exposure at a high concentration (48h, 1µM) revealed broad transcriptional effects with more than half of the expressed probesets showing significant up- or downregulation (adj. p-value<0.05). Significantly downregulated genes included stem-cell associated genes and putative oncogenes such as BAALC, WT1, MN1, MEF2C, LMO1, LMO2, BCL2, IGFBP7, ZEB2, GFI1B, MYB and LYL1.
2016-12-15 | GSE81917 | GEO
Project description:Gene expression profile of human lung cell line (A549) treated with 2mM 59cobalt chloride during 30mn, 2h, 4h and 24h
| PRJNA97319 | ENA
Project description:Kynureninase is a member of a large family of catalytically diverse but structurally homologous pyridoxal 5'-phosphate (PLP) dependent enzymes known as the aspartate aminotransferase superfamily or alpha-family. The Homo sapiens and other eukaryotic constitutive kynureninases preferentially catalyze the hydrolytic cleavage of 3-hydroxy-l-kynurenine to produce 3-hydroxyanthranilate and l-alanine, while l-kynurenine is the substrate of many prokaryotic inducible kynureninases. The human enzyme was cloned with an N-terminal hexahistidine tag, expressed, and purified from a bacterial expression system using Ni metal ion affinity chromatography. Kinetic characterization of the recombinant enzyme reveals classic Michaelis-Menten behavior, with a Km of 28.3 +/- 1.9 microM and a specific activity of 1.75 micromol min-1 mg-1 for 3-hydroxy-dl-kynurenine. Crystals of recombinant kynureninase that diffracted to 2.0 A were obtained, and the atomic structure of the PLP-bound holoenzyme was determined by molecular replacement using the Pseudomonas fluorescens kynureninase structure (PDB entry 1qz9) as the phasing model. A structural superposition with the P. fluorescens kynureninase revealed that these two structures resemble the "open" and "closed" conformations of aspartate aminotransferase. The comparison illustrates the dynamic nature of these proteins' small domains and reveals a role for Arg-434 similar to its role in other AAT alpha-family members. Docking of 3-hydroxy-l-kynurenine into the human kynureninase active site suggests that Asn-333 and His-102 are involved in substrate binding and molecular discrimination between inducible and constitutive kynureninase substrates.
| S-EPMC2531291 | biostudies-literature