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Homo sapiens

ABSTRACT: Pbx1-d Induces T cell Activation and a Decreased Apoptosis in Response to Retinoic Acids (RA)

OTHER RELATED OMICS DATASETS IN: E-GEOD-22313

PROVIDER: PRJNA127921 | ENA |

REPOSITORIES: ENA

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Pre-B cell leukemia homeobox protein Pbx1 is associated with lupus susceptibility in mice and humans

Project description:Sle1a.1 is part of the Sle1a lupus susceptibility locus which results in the production of activated and autoreactive CD4+ T cells as well as a reduction in the peripheral regulatory T cell (Treg) pool. Sle1a.1 CD4+ T cells showed a defective response to retinoic acid (RA) expansion of TGFβ-induced Tregs. At the molecular level, Sle1a.1 corresponds to an increased expression of a novel splice isoform of Pbx1, Pbx1-d. Pbx1-d over-expression is sufficient to induce an activated/inflammatory phenotype in Jurkat T cells, and to decrease their apoptotic response to RA. PBX1-d is expressed more frequently in lupus patients than in healthy controls, and its presence correlates with an increased memory T cell population. These findings indicate that Pbx1 is a novel lupus susceptibility gene that regulates T cell activation and tolerance.

2010-06-16 | GSE22313 | GEO

Pre-B cell leukemia homeobox protein Pbx1 is associated with lupus susceptibility in mice and humans

Project description:Sle1a.1 is part of the Sle1a lupus susceptibility locus which results in the production of activated and autoreactive CD4+ T cells as well as a reduction in the peripheral regulatory T cell (Treg) pool. Sle1a.1 CD4+ T cells showed a defective response to retinoic acid (RA) expansion of TGFÎ²-induced Tregs. At the molecular level, Sle1a.1 corresponds to an increased expression of a novel splice isoform of Pbx1, Pbx1-d. Pbx1-d over-expression is sufficient to induce an activated/inflammatory phenotype in Jurkat T cells, and to decrease their apoptotic response to RA. PBX1-d is expressed more frequently in lupus patients than in healthy controls, and its presence correlates with an increased memory T cell population. These findings indicate that Pbx1 is a novel lupus susceptibility gene that regulates T cell activation and tolerance. Total RNA from CD4+ T cells from C57BL/6 (B6) and B6.Sle1a.1 (Sle) mice was isolated, with 4 biological replicates each. Gene expression data from C57BL/6 mice were compared with data from B6.Sle2c1 mice.

2010-07-08 | E-GEOD-22313 | biostudies-arrayexpress

Dissecting the retinoid-induced differentiation of F9 embryonal stem cells by integrative genomics [mRNA profiling]

Project description:Retinoic acid (RA) triggers physiological processes by activating heterodimeric transcription factors comprising retinoic acid (RARa,b,g) and retinoid X (RXRa,b,g) receptors. How a single signal induces highly complex temporally controlled networks that ultimately orchestrate physiological processes is unclear. Using an RA-inducible differentiation model we defined the temporal changes in the genome-wide binding patterns of RARg and RXRa and correlated them with transcription regulation. Unexpectedly, both receptors displayed a highly dynamic binding, with different RXRa heterodimers targeting identical loci. Comparison of RARg and RXRa co-binding at RA-regulated genes identified putative RXRa-RARg target genes that were validated with subtype-selective agonists. Gene regulatory decisions during differentiation were inferred from transcription factor target gene information and temporal gene expression. This analysis revealed 6 distinct co-expression paths of which RXRa-RARg is associated with transcription activation, while Sox2 and Egr1 were predicted to regulate repression. Finally, RXRa-RARg regulatory networks were reconstructed through integration of functional co-citations. Our analysis provides a dynamic view of RA signalling during cell differentiation, reveals RA heterodimer dynamics and promiscuity, and predicts decisions that diversify the RA signal into distinct gene-regulatory programs. Transcriptional activity in F9 cells treated with different retinoic acid receptor (RAR) agonists; like all-trans retinoic acid (ATRA), BMS961 (RARg-specific), BMS753 (RARa-specific) or BMS641(RARb-specific); has been evaluated at different time-points (2, 6, 24, 48h) and compared with that found under Ethanol-vehicle treatment conditions (48h treatment).

2011-10-10 | E-GEOD-30537 | biostudies-arrayexpress

Phosphoproteome of RA-responsive and RA-resistant breast cancer cell lines

Project description:Retinoic acid (RA), the main active vitamin A metabolite, controls multiple biological processes such as cell proliferation and differentiation through genomic programs and kinase cascades activation. Due to these properties, RA has proven anti-cancer capacity. Several breast cancer cells respond to the antiproliferative effects of RA, while others are RA-resistant. However, the overall signaling and transcriptional pathways that are altered in such cells have not been elucidated. Here, in a large-scale analysis of the phosphoproteins and in a genome-wide analysis of the RA-regulated genes, we compared two human breast cancer cell lines, a RA-responsive one, the MCF7 cell line, and a RA-resistant one, the BT474 cell line, which depicts several alterations of the "kinome".

2020-10-15 | PXD005911 | Pride

Phosphoproteome of RA-responsive and RA-resistant breast cancer cell lines

2016-07-05 | PXD004357 | Pride

RIME against PBX1 protein in P19.6 mouse embryonal carcinoma cells treated for 48 hours with all-trans retinoic acid

Project description:Identification of PBX1 interactors in P19.6 mouse embryonal carcinoma cells treated for 48 hours with all-trans retinoic acid.

2017-04-03 | PXD006158 | Pride

MicroRNA profiling shows different response to retinoids in estrogen-receptor positive and negative cells

Project description:This Series reports results of miRNA profiling of estrogen-receptor-positive (MCF7) and estrogen-receptor-negative (MDA-MB-231) cells. Retinoic Acid (RA) induces mir-21 in MCF-7 but not in MDA-MB-231 cells. MCF-7 and MDA-MB-231 cells were treated (or not) with retinoic acid (RA) and grown for either 6 hours or 48 hours. miRNA profiling: Factorial design 2x2x2 'cube'; main factors: RA, cells, time; interactions: RA.cells, RA.time, cells.time, RA.cells.time.

2010-05-21 | E-GEOD-18628 | biostudies-arrayexpress

MicroRNA profiling shows different response to retinoids in estrogen-receptor positive and negative cells

2010-05-21 | GSE18628 | GEO

Gene expression from fibroblast-like synoviocytes (FLS) of three patients with rheumatoid arthritis (RA) that were cultured in four conditions: control medium (Basal), ATRA, TNF and ATRA+TNF.

Project description:The aim of this study was to investigate the response of FLS from RA patients to retinoic acid and retinoic acid combined with the central cytokine of RA, TNF.

2019-12-09 | GSE120785 | GEO

Pbx1-d Induces T cell Activation and a Decreased Apoptosis in Response to Retinoic Acids (RA)

Project description:The hypothesis was tested that the Pbx1-d isoform was responsible for the Sle1a.1 phenotypes in CD4+ T cells. Jurkat T cells were transfected with a lentiviral construct expressing Pbx1-d-GFP or control RFP. Pbx1-d over-expression reduced the percentage of late apoptotic cells in response to anti-CD3 and anti-CD28 stimulation as compared with control-Lin28-transfected cells. Overall, these data demonstrate that over-expression of Pbx1-d results in an activated/inflammatory phenotype and in a defective response to RA in Jurkat T cells, strongly suggesting that the increased expression of Pbx1-d is responsible for the Sle1a.1 phenotypes.

2010-07-07 | GSE22799 | GEO

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