Expression data from 205432- or 206381-treated BE(2)-C cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE51909 | GEO | 2013/10/31
SECONDARY ACCESSION(S): PRJNA225797
REPOSITORIES: GEO
Similar Datasets
Project description:Analysis of transcription response of undifferentiated human BE(2)-C neuronal cells to stimulation with novel indole-2-carboxamide antivirals 205432 or 206381. Independent sets of BE(2)-C cells were treated with 25 uM of either 205432 or 206381, or DMSO as control. Total RNA was harvested at 24 h after stimulation and analyzed with Affymetrix U133 Plus 2.0 chips.
2013-10-31 | E-GEOD-51909 | biostudies-arrayexpress
Project description:Analysis of transcription response of undifferentiated human BE(2)-C neuronal cells to stimulation with purified antimycin A1a or unfractionated commercially available antimycin A (Sigma A8674).
2013-02-22 | GSE44541 | GEO
Project description:Analysis of transcription response of undifferentiated human BE(2)-C neuronal cells to stimulation with purified antimycin A1a or unfractionated commercially available antimycin A (Sigma A8674). Three independent sets of BE(2)-C cells were treated DMSO control or 200 nM of either purified antimycin A1a or unfractionated antimycin A. Total RNA was harvested at 24 h after stimulation and analyzed with Affymetrix U133 Plus 2.0 chips.
2013-02-22 | E-GEOD-44541 | biostudies-arrayexpress
Project description:REST has been initially described as a repressor of neuronal genes in non-neuronal cells by binding to its recognition sequence RE1. Over-activation of this factor has been shown in several diseases such as Huntington disease or central nervous system cancers. High-throughput screening of a library of 6,984 compounds with luciferase-assay measuring REST activity in neural derivatives of human embryonic stem cells led to the identification of one benzoimidazole-5-carboxamide derivative (X5050) that inhibited REST silencing in a RE1-dependent manner. Differential transcriptomic analysis revealed the upregulation of neuronal genes targeted by REST.
2013-10-01 | GSE40695 | GEO
Project description:REST has been initially described as a repressor of neuronal genes in non-neuronal cells by binding to its recognition sequence RE1. Over-activation of this factor has been shown in several diseases such as Huntington disease or central nervous system cancers. High-throughput screening of a library of 6,984 compounds with luciferase-assay measuring REST activity in neural derivatives of human embryonic stem cells led to the identification of one benzoimidazole-5-carboxamide derivative (X5050) that inhibited REST silencing in a RE1-dependent manner. Differential transcriptomic analysis revealed the upregulation of neuronal genes targeted by REST. RNA was extracted from 6 samples, corresponding to 3 independent cultures of NSC SA-01, each one treated either with DMSO (0.1 % final) or with X5050 (100 õM final). RNA was isolated using RNeasy Mini kit with DNase I digestion and genome-wide gene expression profiling was performed by hybridization on Affymetrix microarrays
2013-10-01 | E-GEOD-40695 | biostudies-arrayexpress
Project description:The root cap-specific conversion of the auxin precursor indole-3-butyric acid (IBA) into the main auxin indole-3-acetic acid (IAA) generates a local auxin source which subsequently modulates both the periodicity and intensity of auxin response oscillations in the root tip of Arabidopsis, and consequently fine-tunes the spatiotemporal patterning of lateral roots. To explore downstream components of this signaling process, we investigated the early transcriptional regulations happening in the root tip during IBA-to-IAA conversion in Col-0 and ibr1 ibr3 ibr10 triple mutant after 6 hours of IBA treatment.
2015-05-12 | GSE59426 | GEO
Project description:Altered tryptophan catabolism has been identified in inflammatory diseases like rheumatoid arthritis (RA) and spondyloarthritis (SpA), but the causal mechanisms linking tryptophan metabolites to disease are unknown. Using the collagen-induced arthritis (CIA) model we identify alterations in tryptophan metabolism, and specifically indole, that correlate with disease. We demonstrate that both bacteria and dietary tryptophan are required for disease, and indole supplementation is sufficient to induce disease in their absence. When mice with CIA on a low-tryptophan diet were supplemented with indole, we observed significant increases in serum IL-6, TNF, and IL-1β; splenic RORγt+CD4+ T cells and ex vivo collagen-stimulated IL-17 production; and a pattern of anti-collagen antibody isotype switching and glycosylation that corresponded with increased complement fixation. IL-23 neutralization reduced disease severity in indole-induced CIA. Finally, exposure of human colon lymphocytes to indole increased expression of genes involved in IL-17 signaling and plasma cell activation. Altogether, we propose a mechanism by which intestinal dysbiosis during inflammatory arthritis results in altered tryptophan catabolism, leading to indole stimulation of arthritis development. Blockade of indole generation may present a novel therapeutic pathway for RA and SpA.
2023-11-13 | GSE241655 | GEO
Project description:Transcriptional profiling of Arabidopsis thaliana seedlings treated with auxin (indole-3-acetic acid), highlighting to the physiological function of auxin by observing early response of gene expressions in Arabidopsis seedlings.
2012-05-10 | GSE37899 | GEO
Project description:Purpose: The goal of this study was to identify transcriptional changes in HCT-8 cells treated with indole for 4 or 12 hours. Methods: Confluent HCT-8 monolayers were infected with excysted Cryptosporidium parvum sporozoites for 4 h, after which cells were washed to remove extracellular parasites. Cells were then treated with 1% DMSO in cell culture medium with or without 880 uM indole. RNA was collected in triplicate for each treatment type after 4 h and 12 h of treatment (8 and 16 hours post infection, respectively). Results: When the two time points were combined, indole significantly upregulated 57 genes and downregulated 11 genes. Of the upregulated genes,16 genes were primarily upregulated in cells exposed to indole for 4 h and then went back down by 12 h of exposure. These genes were primarily involved in pathways related to ER stress and the unfolded protein response (UPR). Conversely, 41 genes had higher gene expression after 12 h of indole exposure and were predominantly involved in membrane transport of carboxylic acids and amino acids. Conclusions: Indole treatment causes ER stress and upregulation of membrane transporters in a human adenocarcinoma cell line infected with Cryptosporidium parvum.
2021-10-13 | GSE185652 | GEO
Project description:Neuronal activity causes the rapid expression of immediate early genes that are crucial for experience driven changes to synapses, learning, and memory. Here, using both molecular and genome-wide next generation sequencing methods, we report that neuronal activity stimulation triggers the formation of DNA double strand breaks (DSBs) in the promoters of a subset of early-response genes, including Fos, Npas4, and Egr1. Generation of targeted DNA DSBs within Fos and Npas4 promoters is sufficient to induce their expression even in the absence of an external stimulus. Activity-dependent DSB formation is likely mediated by the type II topoisomerase, Topoisomerase IIb (Topo IIb), and knockdown of Topo IIb attenuates both DSB formation and early response gene expression following neuronal stimulation. Our results suggest that DSB formation is a physiological event that rapidly resolves topological constraints to early-response gene expression in neurons. Generation of sequencing data from ChIP-seq with antibodies against γH2AX and Topo IIβ after neuronal activity stimulation, and RNA-seq after etoposide treatment
2015-06-04 | E-GEOD-61887 | biostudies-arrayexpress