MiRNA expression data from human cell lines (Panc1 cells)
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Robert Haesler
PROVIDER: E-GEOD-37734 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Shared Molecules
Only show the datasets with similarity scores above: 0.5
Threshold
0.5
Similar Datasets
Project description:The experiment aims to identify miRNAs that are regulated in response to TRAIL R1 si-RNA and TRAIL R2 si-RNA. The overall aim of the study was to identify mechanisms by which TRAIL death receptors may contribute to malignancy via inhibition of let-7 maturation.
2013-11-20 | GSE37734 | GEO
Project description:Dysregulation of professional APC has been postulated as a major mechanism underlying Ag-specific T cell hyporesponsiveness in patients with patent filarial infection. To address the nature of this dysregulation, dendritic cells (DC) and macrophages generated from elutriated monocytes were exposed to live microfilariae (mf), the parasite stage that circulates in blood and is responsible for most immune dysregulation in filarial infections. DC exposed to mf for 24–96 h showed a marked increase in cell death and caspase-positive cells compared with unexposed DC, while mf exposure did not induce apoptosis in macrophages. Interestingly, 48 h exposure of DC to mf induced mRNA expression of the pro-apoptotic gene TRAIL and both mRNA and protein expression of TNF-alpha. mAb to TRAIL-R2, TNF-R1, or TNF-alpha partially reversed mf-induced cell death in DC, as did knocking down the receptor for TRAIL-R2 using small interfering RNA. Mf also induced gene expression of BH3-interacting domain death agonist (Bid) and protein expression of cytochrome c in DC; mf-induced cleavage of Bid could be shown to induce release of cytochrome c, leading to activation of caspase 9. Our data suggest that mf induce DC apoptosis in a TRAIL- and TNF-alpha-dependent fashion. Keywords: Dendritic Cell, Parasite, Human, Microfilariae
2008-09-17 | GSE12787 | GEO
Project description:We used microarrays to analyze gene expression changes in liver after treatment of rats with two compounds from drug development (R1, R2) to identify potential effects related to hepatotoxicity. Experiment Overall Design: Compound R1 or R2, or vehicle control, was given for either 24h or 2 weeks (336h) at different doses.
2009-08-09 | E-GEOD-17388 | biostudies-arrayexpress
Project description:3 samples of R1, R2 and R3 bone marrow monocytes were compared from 3 biological replicates in 3 separate experiments. R1, R2 and R3 were sorted from triplicate experiments from pools of mice
2016-11-24 | GSE90471 | GEO
Project description:Dysregulation of professional APC has been postulated as a major mechanism underlying Ag-specific T cell hyporesponsiveness in patients with patent filarial infection. To address the nature of this dysregulation, dendritic cells (DC) and macrophages generated from elutriated monocytes were exposed to live microfilariae (mf), the parasite stage that circulates in blood and is responsible for most immune dysregulation in filarial infections. DC exposed to mf for 24â96 h showed a marked increase in cell death and caspase-positive cells compared with unexposed DC, while mf exposure did not induce apoptosis in macrophages. Interestingly, 48 h exposure of DC to mf induced mRNA expression of the pro-apoptotic gene TRAIL and both mRNA and protein expression of TNF-alpha. mAb to TRAIL-R2, TNF-R1, or TNF-alpha partially reversed mf-induced cell death in DC, as did knocking down the receptor for TRAIL-R2 using small interfering RNA. Mf also induced gene expression of BH3-interacting domain death agonist (Bid) and protein expression of cytochrome c in DC; mf-induced cleavage of Bid could be shown to induce release of cytochrome c, leading to activation of caspase 9. Our data suggest that mf induce DC apoptosis in a TRAIL- and TNF-alpha-dependent fashion. Experiment Overall Design: Microfilariae and human monocyte derived-DCs were cultuted at a multiplicity of infection of 1:1 for 24hrs for four independent donors. Matching samples exposed to media alone were used for controls The four experimental and 4 control samples were then pooled to create one experoimental and one healthy pool used for microarray analysis.
2008-10-25 | E-GEOD-12787 | biostudies-arrayexpress
Project description:TurboID proximity labeling of EFNB1 in steady state (EFNB1+HEK) and under EPHB3 stimulation (EFNB1+EPHB3). Sample identification as follows:
EFNB1+HEK: NB1335 (R1), NB1453 (R2) and NB1490 (R3).
EFNB1+EPHB3: NB1336 (R1), NB1454 (R2) and NB1491 (R3).
YFP+HEK: NB1339 (R1), NB1457 (R2) and NB1494 (R3).
YFP+EPHB3: NB1340 (R1), NB1458 (R2) and NB1495 (R3).
2024-11-07 | MSV000096330 | MassIVE
Project description:We used microarrays to analyze gene expression changes in liver after treatment of rats with two compounds from drug development (R1, R2) to identify potential effects related to hepatotoxicity. The development cpds have been described in: Pierson et al., J Med Chem 52: 3855-62. R1 corresponds to 36, R2 corresponds to 38
2009-07-29 | GSE17388 | GEO
Project description:Mononuclear phagocytes have important functions in regulating tissue injury and regeneration after AKI. We tested the hypothesis that kidney resident macrophages (R2) and infiltrative mononuclear phagocytes (R1) exist in distinct transcriptional subsets that are resolvable by single cell RNA sequencing. A further objective was to identify transcriptional signatures for those subsets. By cell sorting R2 and R1 cells from quiescent and injured mouse kidneys, we found remarkable heterogeneity among intrarenal innate immune cells. We define four subsets of dendritic cells and six subsets of R2 cells and specify differentially expressed genes that identify these cell types. Additionally, we observed subset-specific transcriptional responses to AKI. R2 cells, which express surface phenotype homogeneity, adopt distinct transcriptional programs in the steady state and after injury. Expression of MHC class II and invariant chain genes are decreased in a predominant subset of R2 cells after AKI. In contrast, other macrophage lineage-defining genes such as C1qa, b, and c, are expressed at similar levels across R2 cell subsets and their expression does not change in response to injury. This study has allowed us to identify R2 and R1 subsets that may prove to be therapeutic targets for inhibiting damaging inflammation and fibrosis or promoting tissue regeneration.
2023-09-01 | GSE157338 | GEO
Project description:Cell-and context-specific activities of nuclear receptors may in part be due to distinct coregulator complexes recruited to distinct subsets of target genes. RIP140 (also called NRIP1) is a ligand-dependent corepressor that is inducible with retinoic acid (RA). We have shown previously that silencing of RIP140 enhances RA-induced differentiation and enhances the induction of model RA target genes in human embryonal carcinoma cells (EC). Through use of microarray technology we sought to elucidate in a de novo fashion the global role of RIP140 in RA-dependent signaling. RIP140-dependent gene expression was largely consistent with RIP140 functioning to limit RAR signaling. Few if any genes were regulated in a manner to support a role for RIP140 in â??active repressionâ??. Interestingly, approximately half of the RA-dependent genes were unaffected by RIP140, suggesting that RIP140 may discriminate between different classes of RA target genes. RIP140 silencing also accelerated RA target gene activation and sensitized EC cells to low doses of RA. Together the data suggests that the RIP140-dependent RA target genes identified here may be particularly important in mediating RA-induced tumor cell differentiation. RIP140 may be an attractive target to sensitize tumor cells to retinoid-based differentiation therapy. Experiment Overall Design: The current investigation sought to determine the global effects of RIP140 on RA-dependent and RAâ??independent gene expression. A dose of siRNA of 90 nM was chosen. Twelve independent hybridizations were performed from mRNA isolated from 12 independent samples. One scrambled and two independent RISC-free siRNA transfections and transfections with three distinct RIP140 siRNAs were performed in NT2/D1 cells. Each siRNA treatment was further treated with either 10 μM RA or DMSO control for 24 hours. Hence, the design consisted of four groups, the three siRNA controls treated with vehicle, Group 1; the siRNA controls treated with RA, Group 2; siRNA to RIP140 treated with vehicle, Group 3; and siRNA to RIP140 treated with RA, Group 4 . Experiment Overall Design: The treatments were done in the presence of normal sera, since charcoal absorption of sera removes many small hydrophobic ligands to the nuclear receptor family in addition to retinoids. This measure was taken with the aim to perhaps identify target genes of other nuclear receptors including orphan receptors that could be regulated by RIP140 in the presence of low levels of their cognate ligands. RA treatment of 10 μM for 24 hours was chosen since previous experience with NT2/D1 cells indicated that a reasonably sized set of altered genes would be obtained. In addition, NT2/D1 cells commit to RA-induced differentiation by 48 hours and RIP140 repression enhances and accelerates the effects of RA in these cells. Therefore, the 24-hour time point is well-within the range of the RA commitment â??windowâ?? and a larger percentage of direct RA-target genes could be expect to be uncovered compared to later time points. Experiment Overall Design: Based on the current understanding of the properties of RIP140, a number of potential outcomes were anticipated: 1) RIP140 may limit RA target gene activation by negative-feedback inhibition upon RA addition, 2) RIP140 may participate in â??active repressionâ?? of gene expression upon RA addition, 3) an unexpected outcome that RIP140 may participate in the activation of a subset of target genes, 4) RIP140 may regulate the transcription of target genes of other nuclear receptors or even non-nuclear receptor transcription factors. Experiment Overall Design: Total RNA was purified using RNeasy columns (Qiagen). Hybridizations were performed according to Affymetrix guidelines at the Dartmouth College Microarray Shared Resource using an Affymetrix GeneChip Workstation. Biotin-labeled cRNA was generated from 5 μg of total RNA and hybridized to the Human Genome (HG) U133 Plus 2.0 chip A total of 12 hybridizations were performed comprising 12-independent biologic samples organized into the four groups of three.
2008-04-04 | E-GEOD-7500 | biostudies-arrayexpress
Project description:Bean leaves treated with BTH or water. 126 = control R1, 127 = BTH R1, 128 = control R2, 129 = BTH R2, 130 = control R3, 131 = BTH R3
2019-07-31 | MSV000084162 | MassIVE