Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA285336 | ENA |
REPOSITORIES: ENA
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Project description:S100A6, a member of the S100 protein family, has been described as relevant for cell cycle entry and progression in endothelial cells. The molecular mechanism conferring S100A6's proliferative actions, however, remained elusive. Originating from the clinically relevant observation of enhanced S100A6 protein expression in proliferating endothelial cells in remodeling coronary and carotid arteries, our study unveiled S100A6 as a suppressor of antiproliferative signal transducers and activators of transcription 1 signaling. Discovery of the molecular liaison was enabled by combining gene expression time series analysis with bioinformatic pathway modeling in S100A6-silenced human endothelial cells stimulated with vascular endothelial growth factor A. This unbiased approach led to successful identification and experimental validation of interferon-inducible transmembrane protein 1 and protein inhibitors of activated signal transducers and activators of transcription as key components of the link between S100A6 and signal transducers and activators of transcription 1. Given the important role of coordinated endothelial cell cycle activity for integrity and reconstitution of the inner lining of arterial blood vessels in health and disease, signal transducers and activators of transcription 1 suppression by S100A6 may represent a promising therapeutic target to facilitate reendothelialization in damaged vessels.
2016-11-21 | GSE69380 | GEO
Project description:Life-long blood cell production is governed through the poorly understood integration of cell-intrinsic and -extrinsic control of hematopoietic stem cell (HSC) quiescence and activation. MicroRNAs (miRNAs) coordinately regulate multiple targets within signaling networks making them attractive candidate HSC regulators. We report that miR-126, a miRNA expressed in HSC and early progenitors, plays a pivotal role in restraining cell cycle progression of HSC in vitro and in vivo. miR-126 knockdown using lentiviral sponges increased HSC proliferation without inducing exhaustion, resulting in expansion of mouse and human long-term repopulating HSC. Conversely, enforced miR-126 expression impaired cell cycle entry leading to progressively reduced hematopoietic contribution. In HSC/early progenitors, miR-126 regulates multiple targets within the PI3K/AKT/GSK3β pathway thus attenuating signal transduction in response to extrinsic signals. These data establish that miR-126 sets a threshold for HSC activation and thus governs HSC pool size, demonstrating the importance of miRNA in the control of HSC function. Total RNA was extracted from cord blood Lin- cells and treated with mir126 shRNA or mir126 containing viral particles (and corresponding controls)
2012-11-30 | E-GEOD-40458 | biostudies-arrayexpress
Project description:Jak1 is a ubiquitously expressed tyrosine kinase that transduces extracellular signals from a variety of cytokines and their receptors to downstream signal transducers and activators of transcription (STATs). Since deficiency in Jak1 causes early neonatal lethality, we generated Jak1 conditional knockout mice to study the biological role of this kinase during the development of the mammary gland in adult females
2016-04-08 | GSE79452 | GEO
Project description:Life-long blood cell production is governed through the poorly understood integration of cell-intrinsic and -extrinsic control of hematopoietic stem cell (HSC) quiescence and activation. MicroRNAs (miRNAs) coordinately regulate multiple targets within signaling networks making them attractive candidate HSC regulators. We report that miR-126, a miRNA expressed in HSC and early progenitors, plays a pivotal role in restraining cell cycle progression of HSC in vitro and in vivo. miR-126 knockdown using lentiviral sponges increased HSC proliferation without inducing exhaustion, resulting in expansion of mouse and human long-term repopulating HSC. Conversely, enforced miR-126 expression impaired cell cycle entry leading to progressively reduced hematopoietic contribution. In HSC/early progenitors, miR-126 regulates multiple targets within the PI3K/AKT/GSK3β pathway thus attenuating signal transduction in response to extrinsic signals. These data establish that miR-126 sets a threshold for HSC activation and thus governs HSC pool size, demonstrating the importance of miRNA in the control of HSC function.
2012-11-30 | GSE40458 | GEO
Project description:Type I interferon-regulated gene expression and signaling in murine mixed glial cells lacking signal transducers and activators of transcription 1or 2 or interferon regulatory factor 9
2017-02-09 | E-MTAB-5445 | ExpressionAtlas
Project description:IL-7 regulates homeostatic mechanisms that maintain the overall size of the T cell pool throughout life. We show that, under steady-state conditions, IL-7 signaling is principally mediated by activation of signal transducers and activators of transcription 5 (STAT5). In contrast, under lymphopenic conditions, there is a modulation of STAT1 expression resulting in an IL-7-dependent STAT1 and STAT5 activation. Consequently, the IL-7-induced transcriptome is altered with enrichment of IFN-stimulated genes (ISGs). Moreover, STAT1 overexpression was associated with reduced survival in CD4+ T cells undergoing lymphopenia-induced proliferation (LIP). We propose a model in which T cells undergoing LIP upregulate STAT1 protein, "switching on" an alternate IL-7-dependent program. This mechanism could be a physiological process to regulate the expansion and size of the CD4+ T cell pool. During HIV infection, the virus could exploit this pathway, leading to the homeostatic dysregulation of the T cell pools observed in these patients.
2018-01-01 | GSE106575 | GEO
Project description:To further investigate the potential molecular basis of the protective effects of HSC on irradiation (6.5Gy) damage, gene expression analysis was conducted on rats liver tissues using microarrays.Pre-treatment with HSC prevented differential expression of 66% (1,398 genes) of 2,126 genes differentially expressed in response to radiation. Pathway enrichment analysis indicated that these genes were mainly involved in a total of 32 pathways, such as olfactory transduction, uroactive ligand-receptor interaction, pathways in cancer, calcium signaling pathway, vascular smooth muscle contraction, cytokine-cytokine receptor interaction, mitogen-activated protein kinase (MAPK) signaling pathway, peroxisomal proliferator-activated receptor (PPAR）signaling pathway, gonadotropin-releasing hormone (GnRH) signaling pathway, Wnt signaling pathway, janus kinase-signal transducers and activators of transcription (Jak-STAT) signaling pathway, Notch signaling pathway.Our analysis indicated that the pretreatment of rats with HSC attenuated radiation-induced these pathways, such as multiple MAPK pathways, suggesting that the protective effect of HSC acts mainly through the attenuation of these pathways.
2014-05-15 | GSE57692 | GEO
Project description:To further investigate the potential molecular basis of the protective effects of HSC on irradiation (6.5Gy) damage, gene expression analysis was conducted on rats liver tissues using microarrays.Pre-treatment with HSC prevented differential expression of 66% (1,398 genes) of 2,126 genes differentially expressed in response to radiation. Pathway enrichment analysis indicated that these genes were mainly involved in a total of 32 pathways, such as olfactory transduction, uroactive ligand-receptor interaction, pathways in cancer, calcium signaling pathway, vascular smooth muscle contraction, cytokine-cytokine receptor interaction, mitogen-activated protein kinase (MAPK) signaling pathway, peroxisomal proliferator-activated receptor (PPAR）signaling pathway, gonadotropin-releasing hormone (GnRH) signaling pathway, Wnt signaling pathway, janus kinase-signal transducers and activators of transcription (Jak-STAT) signaling pathway, Notch signaling pathway.Our analysis indicated that the pretreatment of rats with HSC attenuated radiation-induced these pathways, such as multiple MAPK pathways, suggesting that the protective effect of HSC acts mainly through the attenuation of these pathways. The rats were randomly assigned to one of the three following treatment groups (10-12 animals per group): normal control, radiation and HSC dose (10g/kg body weight/day) + radiation. HSC dissolved in double distilled water were administered intragastrically to the male animals for 3 consecutive days before irradiation. Radiation induced gene expression in rat liver was measured at 24 hours after 6.5 Gy exposure.
2014-05-15 | E-GEOD-57692 | biostudies-arrayexpress
Project description:CNTNAP4 signaling regulates osteosarcoma disease progression
| PRJNA865383 | ENA