Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptomic profiling in NUAK1 KO neurons

ABSTRACT: The project focuses on the protein kinase NUAK1, which controls the development of brain cortical connectivity in mice. Recent data suggest that NUAK1 is involved in the regulation of the spliceosome and more broadly of mRNA biology. The aim of this project is to test whether inactivation of NUAK1 (constitutive KO) in primary neuronal cultures affects the expression level of genes relevant for cortical and axon development. We prepared primary cultures of mouse neurons at the embryonic developmental stage E15.5. The samples were either KO or WT (controls). We collected the samples from 4 individual cultures performed blind to genotype, then selected the samples based on PCR to identify sex and genotype. Cultures were thus performed under the same conditions but not performed the same day nor from the same litter for each sample.

ORGANISM(S): Mus musculus

PROVIDER: GSE227203 | GEO | 2024/01/22

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Roles of the kinase NUAK1 on spliceosome in the mouse cortex

Project description:The project focuses on the protein kinase NUAK1, which controls the development of brain cortical connectivity in mice. Recent data suggest that NUAK1 is involved in the regulation of the spliceosome and more broadly of mRNA biology. The aim of this project is to test whether inactivation of NUAK1 (constitutive KO) affects the expression level of genes relevant for cortical development in the embryonic brain. We collected the cortex of embryos (littermates) at the late embryonic developmental stage (E18.5, i.e. just before birth). The samples will be either KO or WT (controls). We collected the samples on the same day, under the same conditions, and as far as possible we made homogeneous groups: same litter, same proportion of males/females.

2024-01-22 | GSE226698 | GEO

In situ depletion of Nuak1 in murine colon tumours

Project description:The aim of the project is to determine the impact of NUAK1 depletion on the transcriptome of in situ colon tumours. Tumours were initiated in Villin-CRE-ER;APC-floxed;DI-shNUAK1 mice, followed by treatment for 1 week with dextran sodium sulphate. 68 days after tumour initiation, NUAK1 shRNAs were induced by doxycycline administration (via gavage), or left un-induced. 6 tumours were harvested from NUAK1 shRNA expressing mice and 6 from controls. RNA was isolated using Qiagen RNEasy and analyzed by Illumina paired-end RNA-SEQ

2018-02-19 | E-MTAB-6265 | biostudies-arrayexpress

Characterize osteocyte transcriptome under control of PPARa

Project description:RNA-seq analysis of transcriptome of osteocytes isolated from femora cortical bone of 5 mo old C57BL6 mice with WT or PPARa KO genotype. Conclusion: In osteocytes, PPARα controls large number of transcripts coding for signaling proteins and osteocyte secretome which regulates development of bone marrow adipose tissue and peripheral fat metabolism.

2023-03-28 | GSE225595 | GEO

Mettl3/m6A promotes translation of pathogenic mRNAs to mediate cystogenesis in mouse models of ADPKD

Project description:Purpose: Determine the differential m6A methylation pattern of Mettl3 between wildtype, Pkd1F/RC-KO and Pkd1F/RC-Mettl3-DKO mouse kidneys. Methods: m6A RNA IP using the Magna MeRIP™ m6A Kit (EMD Millipore, catalog #17-10499) was performed on P18 wildtype, Pkd1F/RC-KO and Pkd1F/RC-Mettl3-DKO mouse kidney samples. Two biological replicate samples from each genotype were sequenced. Each sample was a pool of 6 kidneys of the same genotype. The input samples were also sequenced to obtain mRNA profiles. Results: 133 mRNAs were found to be differentially hypermethylated in the Pkd1-KO kidneys compared to the control kidneys and differentially hypomethylated in the Pkd1-Mettl3-DKO kidneys compared to the Pkd1-KO kidneys. Two key pathogenic mRNAs namely, c-Myc and Avpr2 were identified and validated as Mettl3 targets. The mRNA transcript levels were unchanged between Pkd1-KO and Pkd1-Mettl3-DKO kidneys. Conclusion: Mettl3/m6A promotes translation of pathogenic mRNAs to mediate cystogenesis in mouse models of ADPKD.

2021-02-03 | GSE165956 | GEO

Hepatic Gene Expression in LIRKO Mice

Project description:Control and Liver Insulin Receptor KO mice (LIRKO) were sacrificed in the non-fasted state. RNA was prepared from liver samples and subjected to expression microarray analysis Each array was hybridized with sample derived from 2-3 mice of the same genotype.

2015-02-05 | GSE65624 | GEO

The Fragile X Mental Retardation Protein (FMRP) controls diacylglycerol kinase in neurons

Project description:In this study, we sought to identify the mRNAs associated to FMRP protein in mouse cortical neuron using a cross linking immunoprecipitation and microarray (CLIP-microarray). The mRNAs crosslinked at 254 nm to FMRP in mouse cortical neurons cultured 8 days in vitro (8 DIV) were immunoprecipitated with H120 anti-FMRP (Santa Cruz) and reverse transcribed to labeled cDNAs with Ovation Pico WTA system V2 (Nugen) and hybridized on Mouse Gene 1.0ST (Affymetrix) We analyzed total RNA (Input) and FMRP-CLIPed RNA (Clip) from 10 primary cortical neuron mouse cultures (5 Wt Input, 5 FMR1-KO Input, 5 Wt Clip, 5 FMR1-KO Clip). Array data was processed by Affymetrix Exon Array Computational Tool. No technical replicates were performed.

2016-06-01 | E-GEOD-51649 | biostudies-arrayexpress

Regulatory mechanisms of TSG-6 (TNF-alfa-induced protein-6: Tnfip6)-deficient and wild-type synovial fibroblasts

Project description:BALB/c mice are susceptible to proteoglycan (PG) aggrecan-induced arthritis (PGIA), and the absence of TSG-6 further increases susceptibility and local inflammatory reactions, including neutrophil invasion into the joints. To gain insight into the mechanisms of TSG-6 action, synovial fibroblasts were isolated from wild-type and TSG-6-KO mice, cultured and exposed to various agents affecting either the TSG-6 expression and/or modify the intracellular function of TSG-6. In the present microarray studies, we have identified differences in gene expression by fibroblasts isolated from wild-type or TSG-6-KO mice Keywords: Genetic modification In this study we compared the gene expression profile of 42 fibroblast cultures from mouse synovial samples. Fifteen samples were wild-type and 27 samples were TSG-6 knockout. In these two genotype groups fibroblasts were treated with TNFa, LPS, TSG-6, HA, or HA+TSG-6, and were compared to untreated samples in the same genotype group. We also compared the same treatments between KO and WT.

2011-07-04 | E-GEOD-17160 | biostudies-arrayexpress

Examining Pathogenesis in Genome Instability Associated Neurodegenerative Mouse Model [TotalStranded-RNA-seq]

Project description:To investigate the molecular basis for ataxia in the DNA repair deficient mice we utilized RNA-seq to evaluate the transcriptome of AtmNes-cre;Aptx-/- (and AtmNes-cre;Parp1-/-) cerebellar and cortical tissue. Using total RNA from symptomatic 10-month-old double-mutant mice and littermate controls, we performed the transcriptome analysis. top 1,000 expressed genes in each genotype

2021-12-14 | GSE174840 | GEO

Local inhibition of protein phosphatase 1 by NUAK1 promotes spliceosome assembly and reveals a MYC-sensitive feedback control of transcriptional elongation

Project description:Deregulated expression of MYC induces a dependence on the NUAK1 kinase, but the molecular mechanisms underlying this dependence have not been fully clarified. Here we show that NUAK1 is a predominantly nuclear protein that associates with a network of nuclear protein phosphatase 1 (PP1) interactors and that PNUTS, a nuclear regulatory subunit of PP1, is phosphorylated by NUAK1. Both NUAK1 and PNUTS associate with the splicing machinery. Inhibition of NUAK1 abolishes chromatin association of PNUTS, reduces spliceosome activity and suppresses nascent RNA synthesis. Activation of MYC does not bypass the requirement for NUAK1 for spliceosome activity, but significantly attenuates transcription inhibition. Consequently, NUAK1 inhibition in MYC-transformed cells induces global accumulation of RNAPII both at the pause-site and at the first exon/intron boundary, but does not increase mRNA synthesis. We suggest that NUAK1 inhibition in the presence of deregulated MYC traps non-productive RNAPII due to the absence of correctly assembled spliceosomes.

2020-02-01 | GSE129925 | GEO

Colorectal tumors require NUAK1 for protection from oxidative stress

Project description:NUAK1 is a member of the AMPK family of kinases involved in regulation of cell adhesion, metabolism and stress responses. Our previous analysis revealed a requirement for NUAK1 to sustain viability when MYC is overexpressed. Human colorectal cancer (CRC) shows near uniform overexpression of MYC, suggesting that this cancer may be particularly amenable to NUAK1 inhibition. This work reveals that elevated NUAK1 expression in human CRC correlates with more aggressive disease, lymph node metastasis and reduced overall survival. Deletion of Nuak1 in murine intestines prevented outgrowth of colonic tumors driven by loss of Apc and KRas mutation, while depletion of Nuak1 in pre-existing tumors drove rapid tumor regression. Mechanistically, we show that NUAK1 promotes anti-oxidant gene expression by facilitating nuclear import of NRF2. Deletion or inhibition of NUAK1 renders cells vulnerable to oxidative stress and provision of exogenous anti-oxidants protects cells in culture and colonic tumors in situ from Nuak1 depletion.

2018-02-26 | PXD008229 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data