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RRAD, IL4I1, CDKN1A, and SERPINE1 genes are potentially co-regulated by NF-κB and p53 transcription factors in cells exposed to high doses of ionizing radiation [RNA-Seq]

ABSTRACT: RRAD, IL4I1, CDKN1A, and SERPINE1 genes are potentially co-regulated by NF-κB and p53 transcription factors in cells exposed to high doses of ionizing radiation [RNA-Seq]

PROVIDER: PRJNA434471 | ENA |

REPOSITORIES: ENA

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RRAD, IL4I1, CDKN1A, and SERPINE1 genes are potentially co-regulated by NF-κB and p53 transcription factors in cells exposed to high doses of ionizing radiation [RNA-Seq]

Project description:Cellular response to ionizing radiation involves activation of the p53-dependent pathways and activation of the atypical NF-?B pathway. Mechanisms of the crosstalk between these two transcriptional networks include (co)regulation of common gene targets. Novel genes potentially (co)regulated by p53 and NF-?B were found using high-throughput genomics screening in human osteosarcoma U2-OS cells irradiated with a high dose (4 and 10 Gy). Radiation-induced expression in cells with silenced TP53 or RELA (coding the p65 NF-?B subunit) genes was analyzed by RNA-Seq while radiation-induced binding of p53 and RelA (p65) in putative regulatory regions was analyzed by ChIP-Seq, then selected candidates were validated by qPCR. A subset of radiation-modulated genes whose expression was affected by silencing of both TP53 and RELA, and a subset of radiation-upregulated genes where radiation stimulated binding of both p53 and RelA were identified. Competition for the same transcriptional coactivators of p53 and NF-?B was the most probable mechanism of a frequent antagonistic effect of the TP53 and RELA silencing. However, this mode of regulation was noted for 3 genes where radiation-induced binding of both p53 and RelA was observed, namely IL4I1, SERPINE1, and CDKN1A. This suggested a possibility of a direct antagonistic (co)regulation by both factors: activation by NF-?B and inhibition by p53 of IL4I1, and activation by p53 and inhibition by NF-?B of CDKN1A and SERPINE1. On the other hand, radiation-induced binding of both p53 and RelA was observed in a putative regulatory region of RRAD gene whose expression was downregulated both by TP53 and RELA silencing, which suggested a possibility of direct (co)activation by both factors.

2018-02-17 | GSE110762 | GEO

RRAD, IL4I1, CDKN1A, and SERPINE1 genes are potentially co-regulated by NF-κB and p53 transcription factors in cells exposed to high doses of ionizing radiation [ChIP-Seq]

Project description:Cellular response to ionizing radiation involves activation of the p53-dependent pathways and activation of the atypical NF-κB pathway. Mechanisms of the crosstalk between these two transcriptional networks include (co)regulation of common gene targets. Novel genes potentially (co)regulated by p53 and NF-κB were found using high-throughput genomics screening in human osteosarcoma U2-OS cells irradiated with a high dose (4 and 10 Gy). Radiation-induced expression in cells with silenced TP53 or RELA (coding the p65 NF-κB subunit) genes was analyzed by RNA-Seq while radiation-induced binding of p53 and RelA (p65) in putative regulatory regions was analyzed by ChIP-Seq, then selected candidates were validated by qPCR. A subset of radiation-modulated genes whose expression was affected by silencing of both TP53 and RELA, and a subset of radiation-upregulated genes where radiation stimulated binding of both p53 and RelA were identified. Competition for the same transcriptional coactivators of p53 and NF-κB was the most probable mechanism of a frequent antagonistic effect of the TP53 and RELA silencing. However, this mode of regulation was noted for 3 genes where radiation-induced binding of both p53 and RelA was observed, namely IL4I1, SERPINE1, and CDKN1A. This suggested a possibility of a direct antagonistic (co)regulation by both factors: activation by NF-κB and inhibition by p53 of IL4I1, and activation by p53 and inhibition by NF-κB of CDKN1A and SERPINE1. On the other hand, radiation-induced binding of both p53 and RelA was observed in a putative regulatory region of RRAD gene whose expression was downregulated both by TP53 and RELA silencing, which suggested a possibility of direct (co)activation by both factors.

2018-02-19 | GSE110800 | GEO

RRAD, IL4I1, CDKN1A, and SERPINE1 genes are potentially co-regulated by NF-κB and p53 transcription factors in cells exposed to high doses of ionizing radiation [ChIP-Seq]

Project description:RRAD, IL4I1, CDKN1A, and SERPINE1 genes are potentially co-regulated by NF-κB and p53 transcription factors in cells exposed to high doses of ionizing radiation [ChIP-Seq]

| PRJNA434584 | ENA

RRAD, IL4I1, CDKN1A, and SERPINE1 genes are potentially co-regulated by NF-?B and p53 transcription factors in cells exposed to high doses of ionizing radiation.

Project description: Not available

| S-EPMC6233266 | biostudies-literature

Transcriptome sequencing of Serpine1-overexpression MLE-12 cells

Project description:To determine the function of Serpine1 in alveolar cells, the Serpine1 overexpression plasmid pCI-neo-Serpine1 was constructed and transfected into MLE-12 cells

2022-10-05 | GSE212689 | GEO

SM004 - SARS infection of C57BL6, TIMP1 and Serpine1 knock-out mice.

Project description:This purpose of this experiment was to investigate the transcriptional differences between C57BL6, TIMP1 and Serpine1 knock-out mice infected with SARS MA15 virus. Overview of Experiment: Groups of 20 week old C57BL6, TIMP1 and Serpine1 (PAI1) knock-out mice were infected with SARS MA15 virus. Infections were done at 10^4 PFU or time-matched mock infected. Time points were 4 and 7 d.p.i. There were 2-4 animals/dose/time point. Lung samples were collected for virus load, transcriptional and proteomics analysis. Weight loss and animal survival were also monitored.

2014-02-20 | E-GEOD-51386 | biostudies-arrayexpress

Mouse Lewis lung carcinoma cell line treated with single or fractionated ionizing radiation doses nated ionizing radiation doses

Project description:Mouse Lewis lung carcinoma cell line treated with single or fractionated ionizing radiation doses nated ionizing radiation doses

| PRJNA328036 | ENA

TAF15 protein regulates CDKN1A through miRNAs

2012-12-21 | GSE34470 | GEO

Characterization of gene expression profiles at low and very low doses of ionizing radiation

Project description:The aim of the present study is to analyze by microarray techniques how gene expression is modulated after exposure to low and very low doses of ionizing radiation, to evaluate if the pattern of gene expression shows dose dependence, and to search for putative regulatory mechanisms behind the observed gene-expression modifications.For this, whole blood samples from five healthy donors diluted in IMDM (1:10) were exposed at six doses between 5 and 500 mGy. Total RNA extraction from CD4+ lymphocytes was done at four different post-irradiation times (150, 300, 450 and 600 min). After mRNA amplification, aRNAs were hybridized on 4x44k DNA microarrays. The results indicated that up-regulation were twice than down-regulation. Surprisingly, the number of modulated genes doesn’t seem to change drastically with dose, even at the lowest dose of 5 mGy. Clustering analysis revealed seven gene expression clusters with different dose dependence profiles. The functional analysis showed that the genes which increased their expression with the dose were related to p53 pathway and DNA damage response. This could be observed from 25 mGy, but becomes very clear at doses equal or greater than 100 mGy. On the other hand, genes with a constant modulation of their expression in all the tested doses were related to cellular respiration, ATP metabolic process and chromatin organization. These latter molecular mechanisms seem to be triggered at very low doses (5-25 mGy). In-silico promoter analysis seems to confirm the implication of transcription factors related to the pathways mentioned above.

2013-06-24 | GSE43151 | GEO

TAF15 protein regulates CDKN1A through miRNAs

Project description:TAF15 (formerly TAFII68) is a member of the TET family of RNA and DNA binding proteins whose genes are frequently translocated in sarcomas. Consistent with a functional role in cell viability, TAF15 depletion had a growth-inhibitory effect and increased apoptosis. Interestingly, one of the genes affected by TAF15 depletion is CDKN1A/p21, a key regulator of cell cycle. Here we show that TAF15 down-regulates CDKN1A/p21 expression through a pathway involving miRNAs. We performed a gene expression profiling upon TAF15 knock down by RNA interference.Total RNAs purified from four biological replicates of HeLa GL3 luc cells transfected either with si-TAF15 or control si-LUC were hybridized to the array.

2012-12-21 | E-GEOD-34470 | biostudies-arrayexpress

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