Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA119751 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptional profiling of 1μg/mL dox and 5μM 1NMPP1 treatedT-REx 293 cells expressing either WT or I642G IRE1α vs control.
2014-12-22 | GSE17152 | GEO
Project description:Transcriptional profiling of INS1 cells expressing either WT IRE1α, I642G IRE1α, N906A IRE1α, or spliced XBP1 comparing 1μg/mL dox and 5μM 1NMPP1 treated vs control.
2014-12-22 | GSE17148 | GEO
Project description:The overall cellular response to oxidative stress generated by Ero1M-NM-1 in the lumen of the mammalian endoplasmic reticulum (ER) is poorly characterized. Here, we investigate the effects of overexpressing a hyperactive mutant (C104A/C131A) of Ero1M-NM-1. Using microarray analysis, we demonstrate that the cell reacts to the oxidative challenge caused by Ero1M-NM-1 hyperactivity by turning on the unfolded protein response. Our findings suggest that the hyperoxidation generated by Ero1M-NM-1-C104A/C131A is addressed in the ER lumen and is unlikely to exert oxidative injury throughout the cell. Human embryonic kidney 293 Flp-In T-REx cells (Invitrogen) overexpressing Ero1M-NM-1-WT and Ero1M-NM-1-C104A/C131A were grown in triplicates and expression was either not induced or induced doxycycline (dox) for 24 h. Extracted RNA was hybridized on Affymetrix microarrays and genes with significantly different expression levels between the four categories were identified by a two-way analysis of variance (ANOVA), where the cell line (Ero1M-NM-1-WT or Ero1M-NM-1-C104A/C131A) and induction status (-dox/+dox) were used as the two factors for the p-value calculation.
2012-09-07 | E-GEOD-40601 | biostudies-arrayexpress
Project description:HER2 transduced cells which we will refer to as HER2-DOX –. These cells are 99% GFP positive (i.e., 99% cells have HER2 transduced, un-induced). As a control, we had GFP empty vector transduced MCF10A cells (95% have GFP transduced). Both cell types in triplicates. We had 4 time-points 0h, 30 mins, 4hours, and 7 hours (time duration for which HER2 will be induced). DOX was added to the GFP-MCF10A cells as a control. Only 1ug/ml of DOX was be used.
2023-01-23 | PXD034105 | Pride
Project description:INS1 cells expressing either WT IRE1α, I642G IRE1α, N906A IRE1α, or spliced XBP1 treated with dox and 1NMPP1
| PRJNA119743 | ENA
Project description:RNA-seq data: Baf60c homozygous deletion vs. WT at two time points in cardiac differentiation
| PRJNA255295 | ENA
Project description:Here we exploit the essential process of X-chromosome dosage compensation to elucidate basic mechanisms that control the assembly, genome-wide binding, and function of gene regulatory complexes that act over large chromosomal territories. We demonstrate that a subunit of C. elegans MLL/COMPASS, a gene-activation complex, acts within the dosage compensation complex (DCC), a condensin complex, to target the DCC to both X chromosomes of hermaphrodites and thereby reduce chromosome-wide gene expression. The DCC binds to two categories of sites on X: rex sites that recruit the DCC in an autonomous, sequence- dependent manner, and dox sites that reside primarily in promoters of expressed genes and bind the DCC robustly only when attached to X. We find that DCC mutants that abolish rex-site binding do not eliminate dox-site binding, but instead reduce it to the level observed at autosomal binding sites in wild-type animals. Changes in DCC binding to these non-rex sites occur throughout development and correlate with transcriptional activity of adjacent genes. Moreover, autosomal DCC binding is enhanced by rex-site binding in cis in X-autosome fusion chromosomes. Thus, dox and autosomal sites exhibit similar binding properties. Our data support a model for DCC binding in which low-level DCC binding at dox and autosomal sites is dictated by intrinsic properties correlated with high transcriptional activity. Sex-specific DCC recruitment to rex sites then greatly elevates DCC binding to dox sites in cis, which lack intrinsically high DCC affinity on their own. We also show here that the C. elegans DCC achieves dosage compensation through its effects on transcription.
2011-03-01 | GSE25833 | GEO
Project description:Here we exploit the essential process of X‐chromosome dosage compensation to elucidate basic mechanisms that control the assembly, genome‐wide binding, and function of gene regulatory complexes that act over large chromosomal territories. We demonstrate that a subunit of C. elegans MLL/COMPASS, a gene-activation complex, acts within the dosage compensation complex (DCC), a condensin complex, to target the DCC to both X chromosomes of hermaphrodites and thereby reduce chromosome-wide gene expression. The DCC binds to two categories of sites on X: rex sites that recruit the DCC in an autonomous, sequence- dependent manner, and dox sites that reside primarily in promoters of expressed genes and bind the DCC robustly only when attached to X. We find that DCC mutants that abolish rex-site binding do not eliminate dox-site binding, but instead reduce it to the level observed at autosomal binding sites in wild-type animals. Changes in DCC binding to these non-rex sites occur throughout development and correlate with transcriptional activity of adjacent genes. Moreover, autosomal DCC binding is enhanced by rex-site binding in cis in X-autosome fusion chromosomes. Thus, dox and autosomal sites exhibit similar binding properties. Our data support a model for DCC binding in which low-level DCC binding at dox and autosomal sites is dictated by intrinsic properties correlated with high transcriptional activity. Sex-specific DCC recruitment to rex sites then greatly elevates DCC binding to dox sites in cis, which lack intrinsically high DCC affinity on their own. We also show here that the C. elegans DCC achieves dosage compensation through its effects on transcription.
2011-03-01 | GSE25831 | GEO
Project description:Flp-In T-REx-293 cells transfected with non-targeting control siRNA or UPF1-specific siRNA as indicated and used for total RNA-seq.
2022-04-07 | GSE176197 | GEO