RNA sequencing of AP1M1 KO HEK293 and U2OS
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1178584 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31135200_1.fastq.gz | Fastqsanger.gz | |||
| SRR31135200_2.fastq.gz | Fastqsanger.gz | |||
| SRR31135169_1.fastq.gz | Fastqsanger.gz | |||
| SRR31135169_2.fastq.gz | Fastqsanger.gz | |||
| SRR31135170_1.fastq.gz | Fastqsanger.gz |
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Project description:Non-targetting ASOs are commonly used as negative controls in vitro and in vivo. Here, we compare the transcriptomic profile of HEK293 and U2OS, following 3 days treatment with 3 different non-targetting ASOs. In those conditions, we did not find major transcriptomic changes following ASO treatment, confirming that they are appropriate negative controls.
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Project description:CRISPR-Cas9 was used to individually knock out SUMO1 and SUMO2 expression in U2OS cells. The transcriptomes of SUMO1 and SUMO2 knockout (KO) cell lines were analyzed using RNA-sequencing.
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Project description:Transcriptome analysis of total RNA samples from HEK293-PIGS-KO and HEK293-PIGS-UBE2J1-DKO cells. To check whether KO of UBE2J1 upregulates genes of GPI biosthesis pathway, we used microarrays to analyze gene expression change by KO of UBE2J1 and comfirmed that known GPI pathway genes are not changed by ERAD-deficiency.
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Project description:In this study we examined the effects of loss of the MYST histone acetyltransferase TIP60 (KAT5) in mouse embryonic fibroblasts (MEFs), human embryonic kidney cells 293 (HEK293), and human osteosarcoma cells (U2OS) on cell proliferation, BrdU incorporation, cell cycle progression, apoptotic and other forms of cell death, DNA damage, histone acetylation at specific lysine residues and RNA expression levels. This dataset relates to U2OS cells. To assess the effects of loss of TIP60 on RNA levels, RNA-seq was performed on U2OS cells, where the TIP60 gene was mutated by CRISPR/Cas9 technology using single guide RNA #1 (g1/C9), single guide RNA #2 (g2/C9), or guide-only controls (g1 or g2). The expression of the guide RNA was induced with doxycycline treatment for 4 days to induce TIP60 gene mutation in the samples also expressing the Cas9 enzyme.
2022-07-22 | GSE208382 | GEO
Project description:Purpose: The goals of this study are to compare NGS-derived U2OS transcriptome profiling (RNA-seq) To get insight into the downstream signaling of AMPK and to evaluate protocols for optimal high-throughput data analysis Methods: RNA was extracted by using the Direct-zol™ RNA Miniprep Plus Kit (Zymo Research) and evaluated the purity and concentration of the RNA by ultraviolet spectroscopy (NanoDrop). RNA integrity numbers (RIN) were evaluated using the Agilent 2100 Bioanalyzer. RNA sequencing libraries were constructed using 1000 ng of total RNA from each sample and the TruSeqV2 kit from Illumina following manufacturer’s protocol. Illumina NextSeq sequencing and NGS data acquisition were conducted at the UNMC Genomics Core Facility. The libraries were subjected to 75 bp paired-end high-output sequencing using a NextSeq500 sequencer to generate approximately 33.3 to 41.6 million reads per sample. Fastq files were generated using the bc12fastq software, version 1.8.4 and provided to the UNMC Bioinformatics Core facility for further analysis. The original fastq format reads were trimmed and filtered using the fqtirm tool (https://ccb.jhu.edu/software/fqtrim) to remove adapters, terminal unknown bases (Ns) and low quality 3’ regions (Phred score < 30). The trimmed fastq files were processed by our facility’s newly developed standard pipeline utilizing STAR as the aligner and RSEM as the tool for annotation and quantification at both gene and isoform levels. TPM values were used for comparison results (student’s t-test) for all the available genes. The Benjamini-Hochberg (BH) adjusted p values were also provided to adjust for multiple testing-caused false discovery rate (FDR) with significant level of adjusted p value of ≤ 0.05. Comparative analysis of parental U2OS (control) vs. AMPKα-KO and control vs. AMPKα1-2A was performed using Ingenuity Pathway Analysis (IPA) to examine canonical pathways similarly altered in each to designate effects due to dysregulation of CDK1 phosphosites. Results: Comparative analysis of parental U2OS (control) vs. AMPKα-KO and control vs. AMPKα1-2A was performed using Ingenuity Pathway Analysis (IPA) to examine canonical pathways similarly altered in each to designate effects due to dysregulation of CDK1 phosphosites. Canonical pathways influencing actin dynamics such as actin cytoskeleton signaling, ILK signaling, and regulation of actin-based motility by Rho were predicted to be significantly activated. The expression of a multitude of genes involved in promoting cellular movement and migration were increased and several inhibitors of cell movement were diminished in AMPKα-KO and α1-2A cells compared to controls. By examining alterations of downstream gene expression, upstream analysis pinpointed numerous possible upstream regulators. Most of the highestscoring upstream effectors were analogously modulated between AMPKα-KO and α1-2A compared to controls, indicating that loss of phosphorylation of AMPK by CDK1 is comparable to AMPK knockout for alterations seen in these particular pathways. We previously detected stark reduction of p-Histone H3 (S10) in both the AMPKα-KO and α1-2A cells, which led to speculate that this was possibly due to either phosphatase dysregulation leading to hyperdephosphorylation, or perturbation of kinase signaling leading to inadequate phosphorylation of Histone H3. Interestingly, there were eight significantly up- or down-regulated phosphatases found to be changed mutually between the AMPKα-KO and α1-2A cells compared to controls. Furthermore, between the two treatments, the expression levels of ten kinases and two mitosis-associated kinases significantly changed compared to controls. Conclusions: Our study represents the first detailed analysis of AMPK Wild Type, AMPKα-KO and AMPKα1-2A U2OS cell Transcriptomes, with biologic replicates, generated by RNA-seq technology. Our results show that that CDK1 regulates AMPK control of mitotic entry and progression. It remains to be determined which signaling networks or processes CDK1-phosphorylated AMPK utilizes to drive these events.
2019-10-24 | GSE139293 | GEO
Project description:In this study we examined the effects of loss of the MYST histone acetyltransferase TIP60 (KAT5) in mouse embryonic fibroblasts (MEFs), human embryonic kidney cells 293 (HEK293), and human osteosarcoma cells (U2OS) on cell proliferation, BrdU incorporation, cell cycle progression, apoptotic and other forms of cell death, DNA damage, histone acetylation at specific lysine residues and RNA expression levels. This dataset relates to HEK293 cells. To assess the effects of loss of TIP60 on RNA levels, RNA-seq was performed on HEK293 cells, where the TIP60 gene was mutated by CRISPR/Cas9 technology using single guide RNA #1 (g1/C9), single guide RNA #2 (g2/C9), or guide-only controls (g1 or g2). The expression of the guide RNA was induced with doxycycline treatment for 3 days to induce TIP60 gene mutation in the samples also expressing the Cas9 enzyme.
2022-07-22 | GSE208379 | GEO
Project description:Microarray of HEK293-PIGS-KO and HEK293-PIGS-UBE2J1-DKO cells.
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