This SuperSeries is composed of the SubSeries listed below.
Stability of gene expression in human T cells in different gravity environments is clustered in chromosomal region 11p15.4.
Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Dynamic gene expression response to altered gravity in human T cells.
Cell line
View SamplesWe investigated differentially regulated genes in human Jurkat T lymphocytic cells in 20s and 5min microgravity and in hypergravity and compared expression profiles to identify potential gravity-regulated genes and adaptation processes.
Dynamic gene expression response to altered gravity in human T cells.
Cell line
View SamplesWe investigated differentially regulated and stably expressed genes in human Jurkat T lymphocytic cells in 5min simulated microgravity and hypergravity and compared expression profiles to identify gravity-regulated and unaffected genes as well as adaptation processes.
Stability of gene expression in human T cells in different gravity environments is clustered in chromosomal region 11p15.4.
Cell line
View SamplesWe investigated differentially regulated genes in human Jurkat T lymphocytic cells in 20s and 5min microgravity and in hypergravity and compared expression profiles to identify potential gravity-regulated genes and adaptation processes.
Dynamic gene expression response to altered gravity in human T cells.
Cell line
View SamplesThe sequential activation of distinct developmental gene networks governs the ultimate identity of a cell, but the mechanisms by which downstream programs are activated are incompletely understood. The preB-cell receptor (preBCR) is an important checkpoint of B-cell development and essential for a preB-cell to traverse into an immature B-cell. Here, we show that activation of Mef2 transcription factors by preBCR is necessary for initiating the subsequent genetic network. We demonstrate that B-cell development is blocked at the preB-cell stage in mice deficient for Mef2c and Mef2d transcription factors and that preBCR signaling enhances the transcriptional activity of Mef2c/d through phosphorylation by the ERK5 mitogen activating kinase. This activation is instrumental in inducing Krüppel-like factor 2 and several immediate early genes of the AP1 and Egr family. Finally, we show that Mef2 proteins cooperate with the products of their target genes (Irf4 and Egr2) to induce secondary waves of transcriptional regulation. Our findings uncover a novel role for Mef2c/d in coordinating the transcriptional network that promotes early B-cell development. Overall design: RNA-seq experiments were performed from Mef2c/d knockout proB-cells versus control cells to identify genes regulated by Klf2
Essential control of early B-cell development by Mef2 transcription factors.
Specimen part, Subject
View SamplesThe sequential activation of distinct developmental gene networks governs the ultimate identity of a cell, but the mechanisms by which downstream programs are activated are incompletely understood. The preB-cell receptor (preBCR) is an important checkpoint of B-cell development and essential for a preB-cell to traverse into an immature B-cell. Here, we show that activation of Mef2 transcription factors by preBCR is necessary for initiating the subsequent genetic network. We demonstrate that B-cell development is blocked at the preB-cell stage in mice deficient for Mef2c and Mef2d transcription factors and that preBCR signaling enhances the transcriptional activity of Mef2c/d through phosphorylation by the ERK5 mitogen activating kinase. This activation is instrumental in inducing Krüppel-like factor 2 and several immediate early genes of the AP1 and Egr family. Finally, we show that Mef2 proteins cooperate with the products of their target genes (Irf4 and Egr2) to induce secondary waves of transcriptional regulation. Our findings uncover a novel role for Mef2c/d in coordinating the transcriptional network that promotes early B-cell development. Overall design: RNA-seq experiments were performed from Blnk-/- preB-cells with an integration of BLNK-ERt2 to identify genes regulated after preBCR signaling
Essential control of early B-cell development by Mef2 transcription factors.
Specimen part, Subject, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Enhancing dopaminergic signaling and histone acetylation promotes long-term rescue of deficient fear extinction.
Sex, Specimen part
View SamplesThe sequential activation of distinct developmental gene networks governs the ultimate identity of a cell, but the mechanisms by which downstream programs are activated are incompletely understood. The preB-cell receptor (preBCR) is an important checkpoint of B-cell development and essential for a preB-cell to traverse into an immature B-cell. Here, we show that activation of Mef2 transcription factors by preBCR is necessary for initiating the subsequent genetic network. We demonstrate that B-cell development is blocked at the preB-cell stage in mice deficient for Mef2c and Mef2d transcription factors and that preBCR signaling enhances the transcriptional activity of Mef2c/d through phosphorylation by the ERK5 mitogen activating kinase. This activation is instrumental in inducing Krüppel-like factor 2 and several immediate early genes of the AP1 and Egr family. Finally, we show that Mef2 proteins cooperate with the products of their target genes (Irf4 and Egr2) to induce secondary waves of transcriptional regulation. Our findings uncover a novel role for Mef2c/d in coordinating the transcriptional network that promotes early B-cell development. Overall design: RNA-seq experiments were performed from Klf2 overexpressing BMiFLT3 (15-3) cells to identify genes regulated by Klf2
Essential control of early B-cell development by Mef2 transcription factors.
Specimen part, Cell line, Subject
View SamplesBackground: Extinction-based exposure therapy is used in treating anxiety- and trauma-related disorders, however there is the need to improve its limited efficacy in individuals with impaired fear extinction learning and to facilitate the inadequate protection against return-of-fear phenomena.
Enhancing dopaminergic signaling and histone acetylation promotes long-term rescue of deficient fear extinction.
Sex, Specimen part
View Samples