RNA-sequencing analysis of mouse liver with a global ERK1, hepatocyte-specific ERK2 or double ERK1/2 knockout
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PROVIDER: PRJNA753503 | ENA |
REPOSITORIES: ENA
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Project description:The analysis examined the effects of a global ERK1 and/or tamoxifen-inducible, hepatocyte-specific ERK2 knockout on the liver transcriptome. Transcriptomes from the livers with a ERK1/2 double knockout were compared to the livers of mice with an ERK1 or ERK2 knockout.
2021-08-13 | GSE181803 | GEO
Project description:Angiogenesis is a complex process orchestrated by both growth factors and cell adhesion to the extracellular matrix and is initiated by focal degradation of the vascular basement membrane with subsequent migration and proliferation of endothelial cells (EC). The Ras/Raf/MEK/ERK pathway is critical for EC function during angiogensis. Although in vitro studies implicate ERK1 and ERK2 in EC survival, their precise role in EC function in vivo remains poorly defined. Cre/loxP technology was used to inactivate Erk1 and Erk2 in EC during murine development, resulting in embryonic lethality due to a drastic reduction in angiogenesis. The angiogenic defect was linked to diminished EC proliferation and migration, but not to increased cell apoptosis. Expression of key cell cycle regulators was diminished in the double knockout cells. In addition, both Paxillin and Focal Adhesion Kinase were expressed at lower levels and failed to correctly localize to the cell membrane in EC lacking Erk1 and Erk2, leading to defects in the organization of the cytoskeleton and in cell motility. The results demonstrate that ERK1 and ERK2 coordinate cell proliferation and migration during angiogenesis. Lentivirus infected cells to generate ERK1/2 WT and ERK1/2 DKO endothelial cells were cultured, RNA was extracted and Affymetrix gene expression arrays were performed.
2010-07-30 | E-GEOD-16967 | biostudies-arrayexpress
Project description:Angiogenesis is a complex process orchestrated by both growth factors and cell adhesion to the extracellular matrix and is initiated by focal degradation of the vascular basement membrane with subsequent migration and proliferation of endothelial cells (EC). The Ras/Raf/MEK/ERK pathway is critical for EC function during angiogensis. Although in vitro studies implicate ERK1 and ERK2 in EC survival, their precise role in EC function in vivo remains poorly defined. Cre/loxP technology was used to inactivate Erk1 and Erk2 in EC during murine development, resulting in embryonic lethality due to a drastic reduction in angiogenesis. The angiogenic defect was linked to diminished EC proliferation and migration, but not to increased cell apoptosis. Expression of key cell cycle regulators was diminished in the double knockout cells. In addition, both Paxillin and Focal Adhesion Kinase were expressed at lower levels and failed to correctly localize to the cell membrane in EC lacking Erk1 and Erk2, leading to defects in the organization of the cytoskeleton and in cell motility. The results demonstrate that ERK1 and ERK2 coordinate cell proliferation and migration during angiogenesis.
2010-07-01 | GSE16967 | GEO
Project description:Activation of ERK1 and ERK2 is essential in regulation of a wide variety of cellular and physiological processes. In native inner medullary collecting ducts, vasopressin (AVP) working through the V2 subtype vasopressin receptor (V2R)-mediated activation of Gαs, inhibits ERK1 and ERK2 activity. However, it has been reported that V2R can signal independently of Gαs through the activation of β-arrestin, which activates ERK1 and ERK2. Vaptans, V2R antagonists that function as so-called “inverse agonists”, have the potential of promoting cell proliferation via β-arrestin-dependent ERK activation. Here we use the mpkCCD cell line which natively expresses V2R to investigate the effects of AVP, the V2-selective analog dDAVP, and tolvaptan on ERK1 and ERK2 phosphorylation and activation. We demonstrated that ERK1 and ERK2 phosphorylation in mpkCCD cells was significantly reduced by either AVP or dDAVP, in contrast to the increases seen in non-collecting duct cells overexpressing V2R. We also found that tolvaptan has a strong effect to increase ERK1 and ERK2 phosphorylation in the presence of dDAVP and that the tolvaptan effect to increase ERK1 and ERK2 phosphorylation is absent in PKA-null mpkCCD cells. Thus, it appears that the tolvaptan effect to increase ERK activation is PKA-dependent and, therefore, not mediated by the β-arrestin pathway. Overall, the studies show that AVP decreases and that tolvaptan increases ERK1 and ERK2 activation in cells expressing V2R at endogenous levels, and provide no evidence for a role for β-arrestin in the regulation of ERK1 and ERK2 activity.
2023-11-17 | GSE243773 | GEO
Project description:We knocked out ERK1 and ERK2 in the striatopallidal population of striatal medium spiny neurons and analyzed differences in gene expression at P17, a time of increased synapse formation. We used whole gene microarray to assess transcriptional changes that occur in the mouse striatum at P17 in response to ERK1/2 deletion in striatopallidal medium spiny neurons.
2017-07-25 | GSE93844 | GEO
Project description:We assessed the effect of RNAi-mediated MAP kinase cascade signaling blockade in primary human keratinocytes. Two sets of siRNA targeting different regions of the Erk1/2 genes were used, enabling identification of off-target siRNA effects. Primary human keratinocytes were electroporated with scrambled control siRNA, a pair of siRNA oligomers against Erk1 and Erk2 (set A), or an independent pair of siRNA oligomers against Erk1 and Erk2 (set B). Four days after electroporation, RNA was harvested. Three biological replicates were performed for each of the three siRNA groups.
2009-05-03 | E-GEOD-15417 | biostudies-arrayexpress
Project description:ERK1 and ERK2 MAPKs are intensively studied signaling proteins that are involved in numerous cellular processes and signaling networks. However, their specific functions in embryonic development remain elusive. The upstream activation pathways for ERK1 and ERK2 are considered to be highly similar, and also many of their downstream targets are considered as common, but still relatively few in vivo downstream targets of these kinases have been identified conclusively. Recent mice studies indicate distinct roles for both ERKs in cellular proliferation, oncogenic transformation and development. <br><br>Microarray experiments were performed to compare morpholino mediated knockdown of ERK1 versus ERK2 in zebrafish development. These two conditions were compared to a standard control morpholino condition. To exclude possible effects of the control morpholino at a transcriptional level, we also performed the transciptome-analysis of the control morpholino, to an injection control (injection with phenol red).
2008-01-01 | E-MEXP-1163 | biostudies-arrayexpress
Project description:Comparison of unstimulated and in vitro activated wild type and Erk1 or Erk2 deficient CD8 T cells
2008-10-07 | E-MEXP-1833 | biostudies-arrayexpress
Project description:In this study, we provide evidence to show that the expression of PRC2-recruting factor Jarid2 is largely reduced in both naïve mESC and Erk1/Erk2 double knockout (Erk1/2-dKO) mESCs, which can be rescued by reactivation of FGF/MARK signaling in naïve mESCs or ectopic Erk1 expression in Erk1/2-dKO mESCs, suggesting the FGF/ERK signaling positively regulates the Jarid2 expression in mESCs. Consistent with the Jarid2 function in the PRC2 recruitment, the global Ezh2 occupancy and histone H3K27me3 are largely reduced at CpG islands (CGIs) and bivalent promoters in both naïve mESCs and Erk1/Erk2-dKO mESCs, which can be fully restored by ectopic expression of Jarid2 expression, suggesting the reduced Jarid2-mediated PRC2 recruitment is a main molecular mechanism leading to the global reduction of PRC2 occupancy at CpG islands and bivalent promoters in naïve mESCs. At the transcriptional level, although both PRC2 occupancy and histone H3K27me3 modification are reduced at bivalent promoters, there exist two groups of genes with distinct expression status. the FGF/ERK signaling target genes are silenced while the Wnt signaling target genes are largely de-repressed, which is caused by the chemical activation of Wnt/beta-catenin signaling in naïve mESCs. Further ChIP-seq analyses demonstrate an increased occupancy of β-catenin at its activated gene promoters in naïve mESCs. These results suggest the transcriptional activation of bivalent genes in naïve mESCs is predominantly determined by the presence of transcriptional factors but not the status of PRC2 occupancy at gene promoters.
2020-10-13 | GSE157748 | GEO
Project description:In this study, we provide evidence to show that the expression of PRC2-recruting factor Jarid2 is largely reduced in both naïve mESC and Erk1/Erk2 double knockout (Erk1/2-dKO) mESCs, which can be rescued by reactivation of FGF/MARK signaling in naïve mESCs or ectopic Erk1 expression in Erk1/2-dKO mESCs, suggesting the FGF/ERK signaling positively regulates the Jarid2 expression in mESCs. Consistent with the Jarid2 function in the PRC2 recruitment, the global Ezh2 occupancy and histone H3K27me3 are largely reduced at CpG islands (CGIs) and bivalent promoters in both naïve mESCs and Erk1/Erk2-dKO mESCs, which can be fully restored by ectopic expression of Jarid2 expression, suggesting the reduced Jarid2-mediated PRC2 recruitment is a main molecular mechanism leading to the global reduction of PRC2 occupancy at CpG islands and bivalent promoters in naïve mESCs. At the transcriptional level, although both PRC2 occupancy and histone H3K27me3 modification are reduced at bivalent promoters, there exist two groups of genes with distinct expression status. the FGF/ERK signaling target genes are silenced while the Wnt signaling target genes are largely de-repressed, which is caused by the chemical activation of Wnt/beta-catenin signaling in naïve mESCs. Further ChIP-seq analyses demonstrate an increased occupancy of β-catenin at its activated gene promoters in naïve mESCs. These results suggest the transcriptional activation of bivalent genes in naïve mESCs is predominantly determined by the presence of transcriptional factors but not the status of PRC2 occupancy at gene promoters.
2020-10-13 | GSE157747 | GEO