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Expression profiles of the hippocampus of Rsk2-KO mice

ABSTRACT: Coffin–Lowry Syndrome (CLS) is a syndromic form of mental retardation caused by loss of function mutations in the X-linked RPS6KA3 gene, which encodes Rsk2, a serine/threonine kinase involved in spatial memory. We analyzed hippocampal gene expression profiles in Rsk2-KO mice to identify changes in molecular pathways. Total RNA was extracted from hippocampi from 6 KO and 6 WT (littermates) 2-month-old male mice. For each genotype, equivalent amounts of RNA from 2 mice were pooled and processed for hybridization to the genome wide oligonucleotide microarray (Murine 430A 2.0 Affymetrix, 22.000 probe sets). Thus, 3 independent pooled samples were hybridized for each genotype.

ORGANISM(S): Mus musculus

PROVIDER: GSE22137 | GEO | 2010/12/22

SECONDARY ACCESSION(S): PRJNA127575

REPOSITORIES: GEO

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Expression profiles of the hippocampus of Rsk2-KO mice

Project description:Coffin–Lowry Syndrome (CLS) is a syndromic form of mental retardation caused by loss of function mutations in the X-linked RPS6KA3 gene, which encodes Rsk2, a serine/threonine kinase involved in spatial memory. We analyzed hippocampal gene expression profiles in Rsk2-KO mice to identify changes in molecular pathways. Total RNA was extracted from hippocampi from 6 KO and 6 WT (littermates) 2-month-old male mice. For each genotype, equivalent amounts of RNA from 2 mice were pooled and processed for hybridization to the genome wide oligonucleotide microarray (Murine 430A 2.0 Affymetrix, 22.000 probe sets). Thus, 3 independent pooled samples were hybridized for each genotype. We compared hippocampal gene expression profiles from rsk2-KO and normal littermate mice to identify changes in molecular pathways

2010-12-22 | E-GEOD-22137 | biostudies-arrayexpress

RSK2 is a modulator of craniofacial development

Project description:The RSK2 gene is responsible for Coffin-Lowry syndrome, an X-linked monogenic disease associating severe learning deficit andassociated to typical facial and digital abnormalities and skeletal changes. Craniofacial and dental anomalies encountered in this rare disease have been poorly characterized. In this study we explore, through X-Ray microtomographic analysis, the variable craniofacial dysmorphism and dental anomalies present in Rsk2 knockout mice, an animal model of Coffin-Lowry syndrome, as well as in triple Rsk1,2,3 knockout mutants. We report in these mutants the occurrence of a surpernumerary tooth mesial to the first molar. This highly penetrant phenotype is considered as a remnant of evolutionary lost teeth. This possibly leads to the significant reduction of the maxillary diastema. Abnormalities of molar shape were almost restricted to the mesial part of both upper and lower first molars (M1). We also report an expression analysis of the four Rsk genes (Rsk1, 2, 3 and 4) at various stages of odontogenesis in wild-type (WT) mice. Rsk2 was mainly expressed in the mesenchymal, neural crest derived compartment, correlating with proliferative areas of the developing teeth and consistent with a biological function of RSK2 in cell cycle control and cell growth, which when invalidated could be responsible for the dental phenotype. In an attempt to unravel the molecular pathways involved in the genesis of these dental defects, we performed a comparative transcriptomic (DNA microarray) analysis of mandibular wild-type versus Rsk2-/Y molars, and further demonstrated a misregulation of selected genes, using a Rsk2 shRNA knock-down strategy in molar tooth germs cultured in vitro.

2014-01-13 | E-GEOD-51034 | biostudies-arrayexpress

RSK2 is a modulator of craniofacial development

2014-01-13 | GSE51034 | GEO

ERK1/2-RSK2 signaling is a developmental switch required for estrogen homeostasis

Project description:Transcriptomic analysis of the mature ER+ population in the mammary gland revealed enrichment for estrogen-responsive genes in the RSK2-KO compared to the wild type.

2020-09-08 | GSE113323 | GEO

RSK2-regulated gene signature associates with ER+ breast cancer

Project description:We used CRISPR RSK2 knock-out MCF-7 cells to identify RSK2-regulated genes.

2020-06-01 | GSE99707 | GEO

Rsk2 controls synovial fibroblast hyperplasia and the course of arthritis.

Project description:To understand differences in the pathogenesis of synovial hyperplasia during TNF-induced arthritis, we compared the global gene expression of hTNFtg and hTNFtg;Rsk2-/y primary synovial fibroblasts. Murine fibroblast-like synoviocytes (FLS) were isolated from the hind paws of hTNFtg and hTNFtg;Rsk2-/y (background: C57BL/6) 6-9 week-old mice via collagenase digestion. The cells of two mice were pooled and cultivated for at least 3 passages before usage. For characterization, the cells were tested for the surface expression of CD90.2 and VCAM1 by flow cytometric analysis, whereas CD11b as a monocytic marker had to be absent. Total RNA was extracted using the RNeasy Mini kit (Qiagen). The integrity and amount of isolated RNA was assessed for each sample using an Agilent 2100 Bioanalyzer (Agilent, Waldbronn, Germany) and a NanoDrop ND-1000 spectrophotometer (NanoDrop Technologies, Wilmington, DE). Double-stranded complementary RNA was synthesized from 1 M-BM-5g total RNA using Message AmpII Biotin (Ambion, USA). Fifteen micrograms of fragmented cRNA of each sample were hybridized to six MG_U430_2 GeneChips (Affymetrix). Hybridization was performed in a Hybridization Oven 640, and chips were washed and stained in the Fluidics Station 450 (both Affymetrix). Finally, the arrays were scanned with a GeneChip Scanner 3000 using the GCOS software, version 1.4, both Affymetrix. All relevant GCOS data of quality checked microarrays were analyzed with High Performance Chip Data Analysis (HPCDA, unpublished), using the BioRetis database (www.bioretis-analysis.de), as described and validated previously.

2014-12-04 | E-GEOD-52992 | biostudies-arrayexpress

HDXMS of ERK2-RSK2 and ERK2-RSK2-ORF45 complexes

Project description:Hydrogen deuterium exchange mass spectrometry data of the ERK2-RSK2 and ERK2-RSK2-ORF45 complexes. The noncatalytic viral protein ORF45 reconfigures ERK-RSK signaling in cells. This dataset identifies the ORF45-RSK2 interface.

2021-12-22 | MSV000088607 | MassIVE

The effects on oncogenic pathway, signaling, by RSK2 N-terminal kinase inhibitor (BI-D1870) in Mantle cell lymphoma-derived cell lines.

Project description:RSK2 is a serine/threonine kinase downstream signaling mediator in the RAS/ERK signaling pathway and may be a therapeutic target in mantle cell lymphoma (MCL). RSK2-Ser227 in the N-terminal kinase domain (NTKD) of RSK2 was found to be ubiquitously active in five MCL-derived cell lines and in tumor tissues derived from five MCL patients. BI-D1870, an inhibitor specific to RSK2-NTKD, caused RSK2-Ser227 dephosphorylation, and thereby, induced dose-dependent growth inhibition via G2/M cell cycle blockade and apoptosis. Comparative gene expression profiling of the MCL-derived cell lines showed that inhibition of RSK2-Ser227 by BI-D1870 caused downregulation of oncogenes, such c-MYC and MYB; anti-apoptosis genes, such as BCL2 and BCL2L1; genes for B cell development, including IKZF1, IKZF3 and PAX5; and genes constituting the B cell receptor signaling pathway, such as CD19, CD79B and BLNK. These findings show that targeting of RSK2-Ser227 enables concomitant blockade of pathways that are critically important in B cell tumorigenesis.

2020-03-25 | GSE147484 | GEO

Rsk2 controls synovial fibroblast hyperplasia and the course of arthritis.

2014-12-04 | GSE52992 | GEO

β-Trcp and RSK2-mediated ubiquitination of FOXN3 facilitates BRCA1-dependent DNA damage repair in lung cancer

Project description:Radioresistance is one of the main factors that lead to the failure of radiotherapy in lung cancer patients. The mechanisms underlying these processes are, however, not fully understood. Here, we find that the low levels of FOXN3 protein is associated with poor prognosis of lung cancer patients. Furthermore, we show that depletion of FOXN3 promotes DNA damage repair and confers lung cancer radioresistance in a BRCA1-dependent manner. Mechanistically, we uncover that E3 ligase β-Trcp and protein kinase RSK2 bind to and cooperatively induce the ubiquitin-mediated degradation of FOXN3. More importantly, β-Trcp and RSK2-mediated ubiquitination of FOXN3 facilitate DNA damage repair in lung cancer. Thus, our findings reveal the molecular mechanism to control the abundance of FOXN3 in DNA damage repair, indicating that targeting β-Trcp/RSK2/FOXN3/BRCA-1 axis may be a novel radiosensitization strategy in lung cancer.

2023-06-30 | GSE218171 | GEO

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