Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE132704 | GEO | 2019/10/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Gene expression in HeLa cells expressing GFP-IRF3 (non-targeting control and clonal knockouts of DDX58, MAVS, ATP13A1, CAPN15, TADA2B, MED16, and MED24) following Sendai virus (SeV) infection or hpRNA transfection

Project description:IRF3 translocates from the cytoplasm to the nucleus upon recognition of a cytoplasmic RNA stimulus by RIG-I or MDA5. Using an optical pooled CRISPR knockout screen in HeLa-Cas9 cells, we identified ATP13A1, CAPN15, TADA2B, MED16, and MED24 as novel genes affecting the translocation of IRF3 upon Sendai virus infection. We generated isogenic clonal knockout HeLa-Cas9 lines and confirmed that loss of these five novel genes results in either decreased (ATP13A1 and CAPN15) or increased (TADA2B, MED16, and MED24) translocation of IRF3 upon Sendai virus or synthetic hpRNA stimulation.

2023-03-05 | GSE179288 | GEO

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

| PRJNA548788 | 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 ablation promotes anti-tumor function by enhancing tumor intrinsic immunogenicity in Pancreatic ductal adenocarcinoma [CUT&Tag]

Project description:Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers with limited treatment options, including checkpoint blockade (ICB) immunotherapy. Epigenetic dysregulation is a defining feature of tumorigenesis and contributes to immune escape. However, little is known about whether and how epigenetic regulators evade immune surveillance in PDAC. Here, we identified Med12, a subunit of RNA polymerase II, as a mediator of immune escape in PDAC with in vivo CRISPR-Cas9 Screening. In murine PDAC models, Med12 loss effectively promoted infiltration and cytotoxicity of CD8+ T cells and NK cells，thereby sensitized to ICB and led to a marked extension of survival. Mechanistically, Med12 loss derepressed endogenous retroelements via impairing H3K9me3 and increasing H3K27Ac modification, triggering cytosolic RNA-sensing and DNA-sensing pathways as well as the type I interferon pathways. Moreover, Med12 depletion induced H3K27Ac gain in the Med12-binding domains, further enhanced the interferon-related genes transcription. Our results demonstrated the role of Med12 in suppressing tumor-intrinsic immunogenicity, thus provided a potential target or marker for immunotherapy of PDAC.

2023-11-30 | GSE242097 | GEO

Med12 ablation promotes anti-tumor function by enhancing tumor intrinsic immunogenicity in Pancreatic ductal adenocarcinoma [ATAC-seq]

2023-11-30 | GSE242080 | GEO

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

Med12 ablation promotes anti-tumor function by enhancing tumor intrinsic immunogenicity in Pancreatic ductal adenocarcinoma [mouse RNA-seq]

2023-11-30 | GSE242096 | GEO

Med12 ablation promotes anti-tumor function by enhancing tumor intrinsic immunogenicity in Pancreatic ductal adenocarcinoma [human RNA-seq]

2023-11-30 | GSE242083 | 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

Histone chromatin modifications in control and Med12-deficient mouse HSPCs

Project description:Using iChIP, we map H3K27Ac, H3K4me3 and H3K4me1 in small populations (HSPCs) in the presence or absence of Med12 and identify affected super-enhancers. iChIP was performed using previously published protocols (Lara-Astiaso et al, 2014 Immunogenetics. Chromatin state dynamics during blood formation - Science, 345, 6199) Examination of histone modification in mouse HSPCs with and without Med12

2016-08-25 | E-GEOD-76052 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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