RNA-seq of human U2OS cells depleted of NUAK1 by shRNA compared to control
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB23631 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR2204770_1.fastq.gz | Fastqsanger.gz | |||
| ERR2204770_2.fastq.gz | Fastqsanger.gz | |||
| ERR2204765_1.fastq.gz | Fastqsanger.gz | |||
| ERR2204765_2.fastq.gz | Fastqsanger.gz | |||
| ERR2204766_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
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Project description:Aim: To determine the impact of NUAK1 depletion on the transcriptome of U2OS cells.
2018-01-01 | E-MTAB-6244 | biostudies-arrayexpress
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
Project description:Homologous recombination-mediated DNA repair deficiency (HRD) predisposes to cancer development, but also provides therapeutic opportunities. Here, we identified an HRD gene signature that robustly predicted HRD status. Unexpectedly, concurrent loss of PTEN in BRCA1-deficient cells might extensively rewire the HR repair network and confer resistance to PARP inhibitor, partially through over-expression of TTK. We used the HRD gene signature as a drug discovery tool and found several PARP-inhibitor-synergizing agents through the connectivity map. Thus gene expression profiling can be used to define the functional status of the HR repair network providing prognostic and therapeutic information. Various shRNAs that target genes involved in homologous recombination (HR) were transfected in MCF-10A non-transformed breast cells lines. Stable HR gene knockdown MCF-10A cells were seeded 200000 at 10 cm plate. Cells were harvested after 48 hours culturing and used for gene expression profiling. The shRNA that target CHK1 gene was transfected in human osteosarcoma U2OS cell line by lentiviral particles and selected stable CHK1 knockdown U2OS cells. Scrambled control shRNA-transfected U2OS cells were applying as control. Both stable CHK1 knockdown and control U2OS cells were seeded with 2 x 10^5 cells at 10 cm culture plate. Cells were cultured in McCOY 5A medium with 10% FBS and harvested after 48 hours culturing. mRNA was extracted from collected cells and performing gene expression profiling. Three biological replicates were applied.
2014-01-24 | E-GEOD-54267 | biostudies-arrayexpress
Project description:RNA-seq of human U2OS cells depleted of NUAK1 by shRNA compared to control
2019-09-09 | E-MTAB-6244 | ExpressionAtlas
Project description:NUDT5 was reported to generate ATP to support local chromatin remodeling and transcription of hormone-responsive genes. Our research has found that NUDT5 is also required for DNA damage repair by homologous recombination. To investigate how NUDT5 regulates HR, we depleted NUDT5 in U2OS cells by siRNA and compared the transcriptome profiling (RNA-seq) of NUDT5 depleted cells with control cells to investigate whether NUDT5 regulate HR by altering the expression of essential components of the HR machinery. The results suggest that NUDT5 does not regulate HR by altering the expression of essential components of the HR machinery. To investigate whether NUDT5 contributes to chromatin remodeling after DNA damage, we compared the chromatin accessibility profiling (ATAC-seq) in NUDT5 depleted U2OS cells and control cells, either before or after ionizing radiation. The results suggest that NUDT5 silencing blocked most DNA damage-induced changes in chromatin accessibility following radiation exposure and implies that NUDT5 may support the activity of remodeling ATPases during damage repair.
2023-02-14 | GSE196718 | GEO
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
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) 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.
2024-01-22 | GSE227203 | GEO
Project description:NUDT5 was reported to generate ATP to support local chromatin remodeling and transcription of hormone-responsive genes. Our research has found that NUDT5 is also required for DNA damage repair by homologous recombination. To investigate how NUDT5 regulates HR, we depleted NUDT5 in U2OS cells by siRNA and compared the transcriptome profiling (RNA-seq) of NUDT5 depleted cells with control cells to investigate whether NUDT5 regulate HR by altering the expression of essential components of the HR machinery. The results suggest that NUDT5 does not regulate HR by altering the expression of essential components of the HR machinery. To investigate whether NUDT5 contributes to chromatin remodeling after DNA damage, we compared the chromatin accessibility profiling (ATAC-seq) in NUDT5 depleted U2OS cells and control cells, either before or after ionizing radiation. The results suggest that NUDT5 silencing blocked most DNA damage-induced changes in chromatin accessibility following radiation exposure and implies that NUDT5 may support the activity of remodeling ATPases during damage repair.
2023-02-14 | GSE196722 | GEO
Project description:NUDT5 was reported to generate ATP to support local chromatin remodeling and transcription of hormone-responsive genes. Our research has found that NUDT5 is also required for DNA damage repair by homologous recombination. To investigate how NUDT5 regulates HR, we depleted NUDT5 in U2OS cells by siRNA and compared the transcriptome profiling (RNA-seq) of NUDT5 depleted cells with control cells to investigate whether NUDT5 regulate HR by altering the expression of essential components of the HR machinery. The results suggest that NUDT5 does not regulate HR by altering the expression of essential components of the HR machinery. To investigate whether NUDT5 contributes to chromatin remodeling after DNA damage, we compared the chromatin accessibility profiling (ATAC-seq) in NUDT5 depleted U2OS cells and control cells, either before or after ionizing radiation. The results suggest that NUDT5 silencing blocked most DNA damage-induced changes in chromatin accessibility following radiation exposure and implies that NUDT5 may support the activity of remodeling ATPases during damage repair.
2023-02-14 | GSE196721 | GEO
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