RNA-sequencing analysis of mouse liver with a global ERK1, hepatocyte-specific ERK2 or double ERK1/2 knockout
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE181803 | GEO | 2021/08/13
REPOSITORIES: GEO
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Project description:RNA-sequencing analysis of mouse liver with a global ERK1, hepatocyte-specific ERK2 or double ERK1/2 knockout
| PRJNA753503 | ENA
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.
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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: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: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.
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Project description:The expression of miR-592 was found to reduce the malignant potential of Group 3 medulloblastoma cell lines, D283, D425 and HD-MB03. RNA-seq analysis was carried out to identify genes differentially expressed upon miR-592 expression in the medulloblastoma cell lines. MiR-592 expression was found to upregulate mTOR and ERK1/ERK2 signaling and bring about neuronal differentiation in D283 and D425 cells. Transcriptome sequencing was also carried out on the RNA extracted from the polyclonal population of D283 and D425 expressing miR-592 as well as the vector control population cells treated with rapamycin or U0126, a MAPK inhibitor to study if the mTOR signaling or MAPK signaling is instrumental in bringing about the neuronal differentiation.
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Project description:The nuclear hormone receptor, estrogen receptor-alpha (ERα), and MAP kinases both play key roles in hormone-dependent cancers, yet their interplay and the integration of their signaling inputs remain poorly understood. In these studies, we document that estrogen-occupied ERα activates and interacts with ERK2, a downstream effector in the MAPK pathway, resulting in ERK2 and ERα colocalization at chromatin binding sites across the genome of breast cancer cells. KEYWORDS: siRNA knock-down, ligand treatment MCF-7 human breast adenocarcinoma cells were tranfected with control, ERK1 and ERK2 siRNA for 60 hours and treated with 0.1% EtOH (Vehicle) or 10 nM E2 for 4 hours or 24 hours, and cDNA microarray analyses were carried out using Affymetrix [HG-U133A_2] Affymetrix Human Genome U133A 2.0 Array.
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