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Timecourse of gene expression in HeLa cells (parental cells and clonal knockouts of MED12 and MED24) following induction by TNFa or IL-1b

ABSTRACT: Timecourse of gene expression in HeLa cells (parental cells and clonal knockouts of MED12 and MED24) following induction by TNFa or IL-1b

PROVIDER: PRJNA548788 | ENA |

REPOSITORIES: ENA

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Timecourse of gene expression in HeLa cells (parental cells and clonal knockouts of MED12 and MED24) following induction by TNFa or IL-1b

Project description:Activation of nuclear factor kappa B (NF-kB) by inflammatory signals results in nuclear translocation of the transcription factor p65 and induction of gene expression. We identified MED12 and MED24 in an optical pooled CRISPR knockout screen in HeLa-Cas9 cells for genes affecting the activation and/or relaxation of p65 to the cytoplasm following induction by either TNFa or IL-1b. We generated isogenic clonal knockout HeLa-Cas9 lines using crRNA transfection and confirmed that loss of MED12 or MED24 results in delayed relaxation of p65, assayed by live-cell imaging of a p65-mNeonGreen fluorescent fusion.

2019-10-01 | GSE132704 | GEO

RNA-seq data of alveolar type 2 epithelial cell derived from organoids treated with IL-1b or TNFa

Project description:Treatment with IL-1b or TNFa enhance the proliferation of alveolar type 2 cells in organoid culture. Here, we examine the downstream mechanisms that enhance AEC2 proliferation after IL-1b and TNFa treatments, we performed RNA-seq analysis of AEC2s isolated from organoids 6 hrs after exposure to either cytokine. We identified 165 differentially expressed genes that were common in both IL-1b and TNFa treated AEC2s compared to saline treated controls.

2019-04-01 | GSE125662 | GEO

SM015 - Infection with SARS MA15 of C57BL/6J mice and Tnfrsf1a/1b knockouts

Project description:Comparing the host response of C57BL/6J mice to Tnfrsf1a/1b knockouts in the same strain of mice.

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Discovery of YAP target genes with TNFa or IL-1b induction

Project description:Proper inflammatory responses are vital to restore tissue homeostasis against offending factors. However, it is largely under explored whether inflammatory responses are modulated by the Hippo effectors YAP/TAZ. To identify the transcription targets related to inflammatory reponses for YAP, we utilized human bronchioalveolar carcinoma cells H358 expressing YAP(5SA) or GFP (as a control) and treated with vehicle, TNFa or IL-1b, respectively. Our work disclosed the complex features of YAP/TAZ’s role in inflammatory responses.

2018-06-02 | GSE115207 | GEO

SM015 - Infection with SARS MA15 of C57BL/6J mice and Tnfrsf1a/1b knockouts

Project description:Comparing the host response of C57BL/6J mice to Tnfrsf1a/1b knockouts in the same strain of mice. Groups of 10-week-old C57BL/6 mice or Tnfrsf1a/1b knockout mice were infected with SARS MA15 at a dose of 10^5 PFU or mock infected. Mice were euthanized on days 4 and 7 post-infection to measure virus load and isolate samples for measurement of virus load, lung pathology, transcriptional analysis and proteomics analysis. Mock-infected animals were also harvested at each time point. Mice were weighed every 24 hours to measure general disease progression and any mouse approaching 30% weight loss was euthanized.

2012-09-13 | E-GEOD-40840 | biostudies-arrayexpress

Discovery of YAP target genes with TNFa or IL-1b induction

Project description:Discovery of YAP target genes with TNFa or IL-1b induction

| PRJNA474112 | ENA

Med12 and p300 chips in HSPCs

Project description:We characterized the genome wide occupancy of Med12 and p300 in mouse HSPCs. We also characterize p300 occupancy upon shRNA against control or Med12. ChIP-seq analysis of Med12 and/or p300 in untreated HSPCs

2016-08-25 | E-GEOD-76053 | biostudies-arrayexpress

Med12 and p300 chips in HSPCs

Project description:We characterized the genome wide occupancy of Med12 and p300 in mouse HSPCs. We also characterize p300 occupancy upon shRNA against control or Med12.

2016-08-25 | GSE76053 | GEO

Total mRNA-seq to determine how the gene expression is altered in both parental and BRCA2-depleted CCNC- and MED12-KO cells.

Project description:Background: Loss of RNA Pol II transcription Mediator components like CCNC, MED12 led to improved survival of PARPi-treated and untreated BRCA2-depleted cells. Mediator is best known for its function with RNA Pol II in regulating gene transcription, we performed total mRNA-Seq with control and BRCA2-depleted CCNC- and MED12-KO cells. The aim of the present prospective study was to reveal how the gene expression is altered in both parental and BRCA2-depleted CCNC- and MED12-KO cells which might contribute to the PARPi resistance in BRCA2 depleted cells. Methods: HEK293A BRCA2 CKI mAID-EGFP WT, CCNC-KO, and MED12-KO with or without BRCA2 depletion cells (each with two biological replicates) were collected and total RNA was extracted and subjected to RNA-seq at HiSeq3000 (Illumina). Results: Based on the transcriptomic data, we examined differentially expressed genes and performed KEGG pathway enrichment analysis.The results suggested that in both control and BRCA2-depleted CCNC- and MED12-knockout cells, several signaling pathways like the transforming growth factor (TGF)-beta signaling pathway and extracellular matrix (ECM)-receptor interaction pathway et al were activated which probably facilitate cell proliferation upon BRCA2 loss. Conclusions: Our results imply that TGF-beta signaling and other signaling pathways such as the ECM-receptor interaction pathway which play roles in the regulation of cellular functions such as proliferation, adhesion, apoptosis, differentiation and migration, may together contribute to the involvement of CCNC and MED12 in drug resistance.

2021-05-06 | GSE150067 | GEO

Genome-wide characterization of MED12 occupancy in human CD34+ cells

Project description:We report ChIP-Seq data for MED12 in human CD34+ cells. Med12 occupies promoter distal regions that regulate specific transcriptional programs required for the homeostasis of the hematopoietic system. 50 milion cells were used to perform ChIP from CD34+ cells with 10 ug of antibody

2016-08-25 | E-GEOD-75914 | biostudies-arrayexpress

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